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63 publications mentioning rno-mir-30b

Open access articles that are associated with the species Rattus norvegicus and mention the gene name mir-30b. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

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[+] score: 242
However, miR-30b overexpression, by transfecting miR-30b agomir, reversed the up-regulation of SCN3A (Figure 2B, [#] P = 0.042) and Nav1.3 (Figure 2C, [#] P = 0.0162) and attenuated the down-regulation of miR-30b (Figure 2A, [###] P < 0.0001). [score:9]
We found that miR-30b directly targeted SCN3A 3′UTR both in vitro and in vivo, and that miR-30b alleviated neuropathic pain by suppressing the expression of Nav1.3 in DRG neurons and spinal cord following SNL. [score:8]
Compared to sham-operated rats, SNL caused an obvious down regulation of miR-30b expression (Figure 3E, [∗∗] P = 0.0013) and up-regulation of Nav1.3 mRNA expression in DRG neurons (Figure 3F, [∗] P = 0.043) as well as in the spinal cord (Figures 3H,I). [score:8]
In addition, we found that miR-30b antagomir transfection up-regulated Nav1.3 (Figures 2E,F), while it down-regulated miR-30b (Figure 2D, [∗] P = 0.014). [score:7]
MiR-30b agomir reversed the upregulation of SCN3A (Figures 6F,I) and downregulation of miR-30b (Figures 6E,H) in SNL rats. [score:7]
Up-Regulation of Nav1.3 Is Inversely Correlated with Down-Regulation of miR-30b in SNL Rats. [score:7]
In western-blot data, the upregulation of Nav1.3 protein was effectively inhibited by miR-30b agomir in DRG neurons (Figure 6G, [∗] P = 0.0303) and spinal cord (Figure 6J, [∗] P = 0.0110) in SNL rats. [score:6]
These findings indicate that miR-30b is involved in the regulation of neuropathic pain by targeting Nav1.3, which might be a potential therapeutic target for neuropathic pain. [score:6]
In the present study, we focused on miR-30b, and we intended to verify whether miR-30b could regulate the expression of Nav1.3, as well as to explore the possibility that miR-30b could potentially alleviate neuropathic pain by changing the expression of Nav1.3 in DRG and the spinal cord Male Sprague–Dawley rats (200–250 g), with food and water ad libitum, were housed in separate cages in a clean and open room with a stable and controlled temperature and a 12 h light–dark cycle. [score:6]
As a consequence, the increased expression of Nav1.3 mRNA and protein and the decreased expression of miR-30b in the DRG and spinal cord of SNL rats confirmed the potential ability of miR-30b to alleviate SNL -induced neuropathic pain. [score:5]
The observed pain-related behaviors were consistently recovered (Figures 3A,C), meanwhile, the increased expression of Nav1.3 was found to reverse (Figures 3F,G,I,J) with intrathecal administration miR-30b agomir in SNL rats, which just verified that a single miRNA was able to act on multiple target genes. [score:5]
Intrathecal miR-30b Agomir Inhibits the Expression of Nav1.3 in DRG and Spinal Cord and Attenuates Neuropathic Pain in SNL Rats. [score:5]
We discovered that SCN3A was the primary target of miR-30b using Target Scan software. [score:5]
The rats were divided into six groups: naïve + scramble (miR-30b inhibitor N. C; 20 μM, 10 μl, GenePharma), naïve + miR-30b antagomir (a selective inhibitor of miR-30b), naïve + scramble (miR-30b agomir N. C), naïve + miR-30b agomir (a selective mimic of miR-30b), SNL + scramble (miR-30b agomir N. C) and SNL + miR-30b agomir. [score:5]
Taken together, we demonstrated that miR-30b suppressed the expression of Nav1.3 mRNA by binding with SCN3A 3′UTR. [score:5]
Using Target Scan software, miR-30b, miR-96, miR-183, and miR-132 were found to target SCN3A. [score:5]
FIGURE 7 Nav1.3 was upregulated by miR-30b antagomir with pain behaviors. [score:4]
Moreover, we found that intrathecal administration of miR-30b antagomir contributed to pain behaviors (Figures 7A,B) and the up-regulation of Nav1.3 (Figures 7E,F, DRG neurons; H,I, spinal cord) in naïve rats. [score:4]
To determine whether miR-30b may regulate the expression of Nav1.3, we used TNF-α (2 μL, 100 ng/mL) to stimulate the primary DRG neurons. [score:4]
FIGURE 1 miR-30b directly targets SCN3A 3′UTR. [score:4]
On the other hand, the role of endogenous miR-30b in regulating Nav1.3 expression was identified in primary DRG neurons. [score:4]
In conformity to previous report (Leinders et al., 2016), intrathecal injection of miR-132-3p mimetic dose -dependently produced pain behavior in naïve rats, miR-132-3p was reported to up-regulated in neuropathic pain, which was in contrast to miR-30b. [score:4]
The finding that Nav1.3 and Nav1.7 were both regulated by miR-30b in neuropathic pain emphasized the importance role of miR-30b in different mo dels of neuropathic pain, implying that miR-30b might be a practicable drug target for the treatment of neuropathic pain. [score:4]
FIGURE 2 miR-30b regulated the expression of Nav1.3 in primary cultured DRG neurons. [score:4]
Down regulation of miR-30b (Figures 7D,G) induced increases in Nav1.3 mRNA in DRG neurons (Figure 7E, [∗∗] P = 0.0011) and in spinal cord (Figure 7H, [∗] P = 0.0344), as well as in protein expression (Figures 7F,I). [score:4]
In accordance with the mRNA level of Nav1.3 in naïve rats, the protein expression of Nav1.3 had no significant change between scramble and miR-30b agomir injected in spinal cord (Figure 7C, P = 0.6914). [score:3]
To determine the expression of miR-30b and Nav1.3 in DRG neurons and the spinal cord of SNL rats, we performed qRT-PCR and western blot analysis (tissues were acquired at day 14 post-SNL surgery). [score:3]
These results confirm that miR-30b overexpression reverses the upward tendency of Nav1.3 in SNL rats at the level of mRNA and protein, leading to a partial easement of pain. [score:3]
Secondly, miR-30b was involved in neuropathic pain by targeting several proteins, and we did not evaluate all of the possible targets of miR-30b. [score:3]
In Figure 5, in situ hybridization results expressed that miR-30b was double-labeled with NF200, IB4, and CGRP (f, i, l). [score:3]
FIGURE 3 Spinal nerve ligation -induced mechanical and thermal allodynia and the change in expression of Nav1.3 and miR-30b. [score:3]
FIGURE 5 Expression distribution of miR-30b and co-localization with Nav1.3 in DRG neurons of naïve rats. [score:3]
To test whether miR-30b agomir could repress the expression of Nav1.3, we measured the expression of miR-30b and Nav1.3 by qPCR and western blot (tissues were acquired at day 14 post-SNL surgeon). [score:3]
Thirdly, Nav1.3 was reported to take part in STZ -induced pain (Tan et al., 2015) and Nav1.7 was changed in inflammatory pain (Yeomans et al., 2005), but whether miR-30b participated in STZ -induced pain or inflammatory pain by targeting SCN3A or SCN9A confused us. [score:3]
MiR-30b Directly Targets SCN3A by Binding with the 3′UTR of SCN3A in PC12 Cells. [score:3]
Intrathecal miR-30b Antagomir Increases the Expression of Nav1.3 in Naïve Rats. [score:3]
To verify whether miR-30b targets SCN3A 3′UTR, a dual luciferase reporter vector containing the sequence of SCN3A 3′UTR was designed (pmirGLO SCN3A 3′UTR). [score:3]
Meanwhile, in naïve rats, it increased miR-30b levels (Figures 6E,H) but had no influence on the expression of SCN3A (P > 0.05). [score:3]
Using Target Scan software, miR-30b, miR-96, mir-183, and miR-132 were predicted to highly relate to SCN3A. [score:3]
MicroRNA-30b regulates expression of the sodium channel nav1.7 in nerve injury -induced neuropathic pain in the rat. [score:3]
However, the luciferase activities of miR-30b antagomir and scrambled miRNAs were unchanged (Figure 1C, P > 0.05), indicating that the inhibition of miR-30b agomir was sequence specific. [score:3]
SCN3A was not only targeted by miR-30b, but also controlled by miR-183 and miR-96 in SNL rat DRGs (Aldrich et al., 2009). [score:3]
The Target Scan software demonstrated that the seed sequence of the miR-30b position (2–8) was paired with SCN3A 3′UTR from 32–39 bps in both humans and rats. [score:3]
To further explore the regulation of Nav1.3 by miR-30b, we down regulated miR-30b by intrathecal injection with miR-30b antagomir in naïve rats. [score:3]
Importantly, the cells containing miR-30b express Nav1.3 in DRG neurons (a–c), indicating a potential interaction between miR-30b and Nav1.3. [score:3]
However, it did address the fact that miR-30b directly regulated SCN3A and further demonstrated that miR-30b had a potential use for the therapy invention for the treatment of neuropathic pain. [score:3]
Moreover, miR-30b agomir transfection increased the expression of miR-30b (Figure 2A, [∗∗∗] P = 0.0010) but did not influence SCN3A (Figure 2B, P = 0.73) or Nav1.3 (Figure 2C, P = 0.75) in untreated DRG cells. [score:3]
Furthermore, increased Nav1.3 levels were inhibited by the transfection of miR-30b agomir (Figure 2B, [#] P = 0.042; Figure 2C, [#] P = 0.0162). [score:3]
These accumulated evidence revealed that miR-30b and SCN3A were crucial players in neuropathic pain, thus, illustrating the potential mechanism would provide a new direction and serviceable theoretical foundation for the clinical intervention of neuropathic pain. [score:2]
FIGURE 6 miR-30b agomir down regulated Nav1.3 and alleviated neuropathic pain. [score:2]
A site-directed gene mutagenesis kit (GenePharma, Shanghai, China) was used to construct the mutant type of the miR-30b binding site vector (pmirGLO-mUTR) according to the protocol provided by the manufacturer. [score:2]
Hence, miR-30b was validated to regulate Nav1.3 at transcription level. [score:2]
Similar to our previous study (Shao et al., 2016), miR-30b was proved to ease neuropathic pain by regulating SCN9A after SNI. [score:2]
During the study, we focused on miR-30b and attempted to explore the potential role of miR-30b and SCN3A in SNL rats. [score:1]
Firstly, the upstream molecules of miR-30b remain uncertain. [score:1]
To assess the exact impact of miR-30b on neuropathic pain, we delivered miR-30b agomir to SNL rats for 4 days following day 10 with intrathecal injection, and 50% PWTs and PWLs were tested. [score:1]
The levels of miR-30b and SCN3A mRNA were measured by qRT-PCR and the changes in Nav1.3 protein expression were determined by western-blot. [score:1]
SCN3A 3′UTR, including the predicted binding sites of miR-30b, was inserted into the 3′UTR region downstream of the firefly luciferase gene of the pmirGLO vector (pmir-GLO-UTR). [score:1]
In the present study, we demonstrated that miR-30b alleviated pain by inhibiting SCN3A through the evaluation of behaviors and changes in molecular levels in SNL rats. [score:1]
In situ hybridization of miR-30b and immunofluorescence staining of NF200 (a–c), IB4 (d–f), CGRP (g–i), and NF200 (j–l) showed that miR-30b was co-localized with nociceptive neuronal and non-nociceptive neurons marker and miR-30b was co-localized with Nav1.3 (a–c), n = 3 rats. [score:1]
30 min later, we transfected miR-30b agomir. [score:1]
Moreover, immunofluorescence and in situ hybridization determined that miR-30b was co-localized with Nav1.3 in rat DRGs (Figure 5), providing evidence for the interaction between miR-30b and Nav1.3. [score:1]
Furthermore, bioinformatics software showed that there are eight nucleotides that match miR-30b and SCN3A 3′UTR. [score:1]
From day 2 following drug administration, the mechanical allodynia (Figure 6A) and thermal hyperalgesia (Figure 6C) caused by SNL were attenuated by intrathecal injection with miR-30b agomir, not scrambled miRNA, but the thresholds of the contralateral hind paw were unchanged (Figures 6B,D, P > 0.05). [score:1]
To further prove the specificity of SCN3A 3′UTR, we transfected mutant 3′UTR plasmid with miR-30b agomir into PC12 cells. [score:1]
As expected, the transfection of scrambled miRNA or mutant SCN3A 3′UTR was not able to change the Firefly/Rellia ratio significantly (Figures 1B,C, P > 0.05), indicating that miR-30b and the 3′UTR of SCN3A were specific. [score:1]
As expected, miR-30b had no effect on luciferase activity (Figure 1C). [score:1]
Through Luciferase assay we verified that miR-30b negatively regulated SCN3A by combining with SCN3A 3′UTR (Figure 1B). [score:1]
We found that the threshold values for mechanical and thermal stimulus were significantly lower during miR-30b antagomir delivery than those of naïve rats injected with scrambled miRNAs (Figures 7A,B), demonstrating that miR-30b antagomir produced pain behaviors in naïve rats. [score:1]
The matched seed sequences between miR-30b-5p and SCN3A 3′UTR were highly conserved between human and rats as shown in Figure 1A. [score:1]
Meanwhile, transfecting miR-30b agomir did not alter the level of SCN3A in naïve DRG neurons (Figure 2C, P = 0.75; Figure 7C, P = 0.6914), which seemed to be ambivalent with the results we acquired from TNF-α treated group or from SNL rats, however, it did match with the characteristics of SCN3A, which was almost undetectable in adult neurons (Estacion et al., 2010), consequently, miR-30b agomir failed to induce changes in the expression of SCN3A in naïve rats. [score:1]
MiR-30b agomir did not affect the baseline of PWTs (Figure 6A) and PWLs (Figure 6C) in naïve rats. [score:1]
We applied miR-30b antagomir to naïve rats for 4 days and determined their sensitivity to mechanical and thermal stimulus. [score:1]
To define the localization of Nav1.3 and miR-30b, double-labeled immunofluorescence and in situ hybridization were performed in DRG neurons. [score:1]
100 μL Neurobasal Medium was used to dilute 5 μL (20 μM) miR-30b agomir/antagomir or 5 μL negative control (20 μM) for 5 min. [score:1]
The special probe sequence for miR-30b was as follows: 5′—AGCTG AGTGT AGGAT GTTTA CA—3′. [score:1]
Even so, the effect of miR-30b antagomir was not unsustainable given the momentariness, along with miR-30b agomir, which have to be settled urgently. [score:1]
One-way ANOVA, n = 3. (C) Transfection of miR-30b agomir with WT SCN3A 3′UTR reduced relative luciferase activity, but no change in luciferase activity was detected in the scramble or mutant SCN3A 3′UTR group, [∗∗∗] P < 0.0001 vs. [score:1]
All SCN3A data were normalized to GAPDH, and all miR-30b data were normalized to u6, which was confirmed to be stable (Zhao et al., 2013; Huang et al., 2016). [score:1]
Transfecting the wild-type plasmid vector with three different doses of miR-30b agomir (10, 50, and 100 pM) into PC12 cells with Lipofectamine 2000, miR-30b agomir reduced relative luciferase activity in a dose -dependent manner (Figure 1B, [∗∗∗] P < 0.0001). [score:1]
After cultivation for 24 h, co-transfection of miRNA mimics (miR-30b agomir; GenePharma, Shanghai, China) at different doses of 10, 50, and 100 pM (50 nmol/L) with wild-type reporter vectors (0.5 μg/mL) was performed with Invitrogen lipofectamine 2000 (Invitrogen, Carlsbad, CA, USA). [score:1]
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[+] score: 219
CaMKIIδ has been reported to regulate VSM proliferation through signaling pathways that result in suppression of p53 and p53-targets including CDKN1 (p21), a cell cycle inhibitor 26. miR-30 family members have been reported to function as tumor suppressors by inhibiting cell proliferation, invasion and inducing apoptosis through different mechanisms, such as targeting BCL9 and repressing Wnt signaling 36. [score:14]
Using well-established aortic VSM primary cell culture and vascular injury mo dels, we demonstrated; 1) an inverse correlation between CaMKIIδ protein and miR-30 family expression in VSM cells upon phenotype switching in vitro and in response to vascular injury in vivo; 2) regulation of CaMKIIδ expression and cell proliferation by miR-30 in cultured VSM with magnitude changes comparable to those observed in vivo following vascular injury; and 3) prevention of CaMKIIδ upregulation with inhibition VSM cell proliferation and neointima formation in vivo following ectopic miR-30 expression. [score:13]
Since we demonstrated that miR-30 significantly inhibited VSM proliferation in vitro, in part by targeting CaMKIIδ expression, we tested effects of ectopic miR-30 expression on CaMKIIδ expression and vascular remo deling in vivo following rat carotid artery balloon injury. [score:11]
Overexpression of miR-30 reduces CaMKIIδ expression by targeting CaMKIIδ mRNA 3′UTR and inhibits VSMCs proliferation. [score:9]
In the present studies, miR-30 overexpression decreased CaMKIIδ expression and inhibited VSM proliferation in vitro, an effect that could be partially rescued by re -expression of CaMKIIδ to physiological levels. [score:9]
Based on reciprocal expression dynamics between CaMKIIδ and miR-30 in VSM in vivo in response to vascular injury, we tested the hypothesis that CaMKIIδ is in fact an endogenous target of miR-30 and its expression is regulated by miR-30. [score:8]
Because the synthetic phenotype cultured VSM cells expressed low levels of miR-30 family members, and effective miR-30 silencing would require siRNAs targeting all of the redundant family members, we relied on gain-of-function approaches to test if CaMKIIδ was, in fact, a direct target for miR-30. [score:8]
Overexpression of miR-30 significantly inhibits CaMKIIδ protein expression in cultured VSMCs. [score:7]
Based on these reports, the current studies, and one report that identified miR-30b as a regulator of CaMKIIδ expression in cardiomyocytes, it is reasonable to propose that dysregulation of a miR-30/CaMKIIδ axis in both VSM and heart might contribute to diverse cardiovascular diseases. [score:7]
CaMKIIδ [2] is involved in miR-30 mediated attenuation of VSM cell proliferationBecause miRs typically have multiple mRNA targets we determined to what extent CaMKIIδ protein expression could rescue miR-30e induced inhibition of VSM proliferation. [score:7]
Additionally, when Shi et al. induced apoptosis using TGF-β in podocytes, miR-30 expression was observed to be down-regulated in a Smad2 -dependent manner 48. [score:6]
Previous studies have suggested coordinate down-regulation of miR-30 family members in skeletal muscle as a function of de-differentiation or dystrophic disease 41, in cardiac muscle as a function of hypertrophy heart failure 42 or atrial fibrillation 43, in human thoracic aortic dissection 44, and in cardiac and VSM cells following ER stress 45 46. [score:6]
Importantly, lentiviral transduction of miR-30 in vivo, immediately following injury, largely prevented subsequent CaMKIIδ upregulation and strongly inhibited VSM cell proliferation and neointimal remo deling. [score:6]
MiR-30 inhibits CaMKIIδ expression by targeting CaMKIIδ 3′UTR in primarily cultured smooth muscle cells. [score:6]
These experiments confirm CaMKIIδ as a target of miR-30 and mediator of miR-30 induced inhibition of cell proliferation. [score:5]
MiR-30 family member expression is significantly decreased following balloon angioplasty injury of rat carotid arteries coincident with CaMKIIδ upregulation and neointimal vascular remo deling. [score:5]
Similarly, comparing miR-30 expression in differentiated VSM from intact aorta medial layers to synthetic phenotype cultured aortic medial VSM cells confirmed reduced expression of miR-30a-e in de-differentiated cells by 30–70%. [score:5]
Partial rescue suggests there are other targets of miR-30 in addition to CaMKIIδ that could be involved in miR-30 induced inhibition of VSM cell proliferation. [score:5]
Given the diversity of pathways impinging on cell cycle control, multiple signaling pathways may also be regulated in VSM by miR-30 and contribute to its net inhibitory effects on VSM proliferation. [score:4]
Deletion of the putative miR-30 binding sequence in the CaMKIIδ 3′-UTR construct abrogated the effects of miR-30, supporting the hypothesis that CaMKIIδ is a direct target for miR-30 in VSM. [score:4]
Neointima formation is a balance between VSMC proliferation and apotosis, and our data does not exclude the possibility that miR-30 regulates VSMC apoptosis in vivo, thus contributing to its inhibitory effect on the neointima formation. [score:4]
How to cite this article: Liu, Y. F. et al. MicroRNA-30 inhibits neointimal hyperplasia by targeting Ca [2+]/calmodulin -dependent protein kinase IIδ (CaMKIIδ). [score:4]
Next, we employed a luciferase reporter assay to determine if miR-30 directly interacts with CaMKIIδ 3′UTR, and exert its inhibitory regulation. [score:4]
miR-30c, the most abundant miR-30 family member in vivo, was introduced into the medial wall by lenti-viral transduction immediately after carotid injury in order to rescue injury -induced miR-30 downregulation. [score:4]
We expect that miR-30, miR-145 and other miRs act collectively to regulate the VSM phenotype switch which involves changes in expression of hundreds of proteins. [score:4]
Thus, it needs to be studied if miR-30 interferes with the activation or promotes differentiation of vascular progenitor cells, resulting in the inhibition of neointima hyperplasia. [score:3]
Lenti-viral delivery of miR-30 to the injured carotid artery walls dramatically inhibits cell proliferation in the medial walls and neointima hyperplasia. [score:3]
Collectively, in differentiated carotid arteries (Fig. 1) and aorta (Fig. 2) miR-30 family members are expressed at levels comparable to miR-145 which is considered a high abundance microRNA associated with and regulating the differentiated VSM phenotype 23. [score:3]
Furthermore, overexpression of miR-30 impairs cultured VSM cell proliferation, and CaMKIIδ rescue in the presence of miR-30 partially, but significantly recovers VSM cell growth. [score:3]
The expression of miR-30 family members is reduced in dedifferentiated vascular smooth muscle. [score:3]
Collectively, miR-30 family members are expressed at a level comparable to miR-145. [score:3]
All miR-30 members were expressed in uninjured carotid medial VSM with miR-30c being the most abundant (Fig. 1d). [score:3]
Based on in silico analysis of the rat CaMKIIδ 3′UTR sequence (TARGETSCAN), a miR-30 family binding sequence is predicted ([+2036]UGUUUACA [+2043]) (Fig. 1c). [score:3]
In summary, we have shown that elevated CaMKIIδ protein and attenuated miR-30 expression in dedifferentiated/synthetic vascular smooth muscle cells in vitro and in vivo. [score:3]
To study if miR-30 binds to CaMKIIδ 3′UTR, full-length of CaMKIIδ 3′UTR (Accession: NM_012519.2, +1825 to +2300) and truncated CaMKIIδ 3′UTR (+1825 to +2035) without miR-30 binding site ([+2036]UGUUUACA [+2043]) were cloned into pMIR-REPORT™ miRNA Expression Reporter Vector (Invitrogen). [score:3]
7 days post vascular injury, expression of all miR-30 family members was significantly reduced in medial wall VSM by 60–80%. [score:3]
Mechanisms underlying coordinate regulation of miR-30 family members are not known. [score:2]
Interestingly, miR-30 family members are encoded on 3 different chromosomes in clustered pairs: miR30a and –c2 on human chromosome 6, miR-30b and-d on chromosome 8, and mir30e and –c1 on chromosome 1. A recent report indicates human coordinate regulation of several miR-30 family members by Mef2 in skeletal muscle 47. [score:2]
Vascular injury induces reciprocal regulation of miR-30 family members and CaMKIIδ protein in rat carotid artery. [score:2]
The expressions of miR-30 family members and miR-145 were compared between injured and uninjured carotid arteries and U6 expression was measured and used for normalization. [score:2]
Moreover, it has been reported that miR-30 regulates epithelial to mesenchymal transition (EMT) and mesenchymal to epithelial transition (MET) in various tumor cells 39 40. [score:2]
MiR-30 inhibits vascular smooth muscle cell proliferation. [score:2]
The significance of the latter experiment is two-fold; confirming miR-30 dependent regulation CaMKIIδ in vivo and suggesting the therapeutic potential for miR-30, at least in the context of restenosis. [score:2]
In the present studies we focused on CaMKIIδ regulation by miR-30 family members which are predicted to bind to a species-conserved sequence in the CaMKIIδ 3′-UTR. [score:2]
CaMKIIδ [2] is involved in miR-30 mediated attenuation of VSM cell proliferation. [score:1]
These magnitude changes are comparable to those previously observed in A10 cells using miR-145 23 and the partial effects in both studies could be due redundant effects of the miR-30 and miR-145 species. [score:1]
A full-length CaMKIIδ 3′UTR construct and truncated CaMKIIδ 3′UTR construct without the predicted miR-30 seed sequence ([+2036]UGUUUACA [+2043]) were cloned into a luciferase reporter vector (Fig. 2c). [score:1]
Upon vascular injury or culture of the VSM cells, total miR-30 levels decrease by approximately 75%, similar in magnitude to the decrease in miR-145 and coincident with the switch to a VSM cell synthetic phenotype. [score:1]
All experiments were carried out with VSM cells from passage 3 to 6. To transduce miR-30 into the common carotid artery wells in vivo, we produced lenti-virus encoding miR-30c using HIV -based pPACKH1 packaging system (System Biosciences, CA, USA). [score:1]
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[+] score: 81
To do this, we injected the neurone -targeted gene knock-down system (LV-mCMV/SYN-tTA + LV-Tretight-GFP-miR30-shRNA/Luc) with LVV to express Luc in astrocytes (LV-GfaABC [1]D-Luc) and, conversely, the astrocyte -targeted knock-down system (LV-mCMV/GfaABC [1]D-tTA+ LV-Tretight-GFP-miR30-shRNA/Luc) together with LVV for neuronal Luc expression (LV-SYN-Luc). [score:11]
LTR, lentiviral long terminal repeats; Tretight, a modified tetracycline and Dox-responsive promoter derived from pTRE-tight (Clontech); GFP, green fluorescence protein; miR30-shRNA/Luc, miR30 -based shRNA targeting firefly Luc gene; miR30-shRNA/nNOS, miR30 -based shRNA targeting rat neuronal nitric oxide synthase gene; Luc, firefly Luc gene; GfaABC [1]D, a compact glial fibrillary acidic protein promoter (690 bp); SYN, human synapsin 1 promoter (470 bp); mCMV, minimal CMV core promoter (65 bp); GAL4BDp65, a chimeric transactivator consisting of a part of the transactivation domain of the murine NF-κBp65 protein fused to the DNA binding domain of GAL4 protein from yeast; WPRE, woodchuck hepatitis post-transcriptional regulatory element. [score:6]
To this end, we constructed a binary Dox-controllable and cell-specific miR30 -based RNAi system to express shRNAs targeting a reporter gene for Luc and an endogenous gene for nNOS. [score:5]
a: LV-mCMV/GfaABC [1]D-tTA controlled miR30-shRNA/Luc didn't knockdown Luc expression in neurones. [score:4]
b: LV-mCMV/SYN-tTA controlled miR30-shRNA/Luc didn't knockdown Luc expression in glia. [score:4]
These results demonstrate that bidirectional transcriptionally amplified SYN and GfaABC [1]D promoters provide a sufficient level of tTA to activate the Tretight promoter which then drives the synthesis of GFP-miR30-shRNA/Luc transcript to induce substantial Luc knock-down. [score:3]
tTA binds to Tretight promoter in LV-Tretight-GFP-miR30-shRNA/Luc and activates the expression of shRNA/Luc. [score:3]
In these constructs gene targeting sequences were embedded in the precursor miRNA context derived from miR30, one of the most well-studied miRNA in mammals. [score:3]
For example, miR-195, miR-497, and miR-30b were found to be enriched in the cerebellum whereas miR-218, miR-221, miR-222, miR-26a, miR-128a/b, miR-138 and let-7c were highly expressed in the HIP. [score:3]
Abbreviation Vector combination Function LVVs-miRLuc-neuroneLV-SYN-Luc+ LV-Tretight-GFP-miR30-shRNA/Luc+ LV-mCMV/SYN-tTA Neurone-specific Luc knock-down system. [score:2]
LVVs-miRnNOS-neuroneLV-Tretight-GFP-miR30-shRNA/nNOS+ LV-mCMV/SYN-tTA Neurone-specific nNOS knock-down system. [score:2]
LVVs-miRLuc-control2LV-GfaABC [1]D-Luc+ LV-Tretight-GFP-miR30-shRNA/Luc + LV-GfaABC1D-WPRE Control combination used in Luc knock-down experiments for the astrocyte-specific system. [score:2]
LVVs-miRnNOS -negative control1LV-Tretight-GFP-miR30-shRNA/Luc+ LV-mCMV/SYN-tTA Negative control combination used in nNOS knock-down experiments for the neurone-specific system. [score:2]
Again, the anti-Luc construct LV-Tretight-GFP-miR30-shRNA/Luc (treatments 4 in Figure 4c and Figure 4d) did not trigger nNOS knock-down. [score:2]
LVVs-miRnNOS-control2LV-Tretight-GFP-miR30-shRNA/nNOS + LV-GfaABC [1]D-WPRE Control combination used in nNOS knockdown experiments for the astrocyte-specific system. [score:2]
LVVs-miRLuc-gliaLV-GfaABC [1]D-Luc+LV-Tretight-GFP-miR30-shRNA/Luc+LV-mCMV/GfaABC1D-tTA Astrocyte-specific Luc knock-down system. [score:2]
LVVs-miRnNOS-control1 LV-Tretight-GFP-miR30-shRNA/nNOS + LV-SYN-WPRE Control combination used in nNOS knockdown experiments for the neurone-specific system. [score:2]
LVVs-miRnNOS-glia LV-Tretight-GFP-miR30-shRNA/nNOS + LV-mCMV/GfaABC1D-tTA Astrocyte-specific Luc knock-down system. [score:2]
Lentiviral systems developed in the course of this study enable tight Dox-controllable and cell-specific miR30 -based RNAi gene knock-down. [score:2]
LVVs-miRLuc-control1LV-SYN-Luc+ LV-Tretight-GFP-miR30-shRNA/Luc+ LV-SYN-WPRE Control combination used in Luc knock-down experiments for the neurone-specific system. [score:2]
LVVs-miRnNOS -negative control2LV-Tretight-GFP-miR30-shRNA/Luc+ LV-mCMV/GfaABC1D-tTA Negative control combination used in nNOS knock-down experiments for the astrocyte-specific system. [score:2]
It is important to note that anti-Luc construct, LV-Tretight-GFP-miR30-shRNA/Luc (treatment 4 in Figure 4a and Figure 4b), was without effect in either cell line, indicating that the nNOS knock-down was sequence-specific. [score:2]
Figure 3Analyses of the efficacy of miR30-shRNA/Luc in vivo in adult rat brain. [score:1]
First, the effect of miR30-shRNA/Luc was assessed in cell lines. [score:1]
To examine whether the different RNAi efficiency in DVC and HIP is caused by different processing of RNAi, we performed northern blotting analysis to assess the ratio between mature -RNAi and precursor-miR30 -RNAi in these two regions. [score:1]
Analysis of the effects of miR30-shRNA/Luc in vivo. [score:1]
We first confirmed the efficacy of the anti-nNOS construct, LV-Tretight-GFP-miR30-shRNA/nNOS in PC12 and 1321N1 cells. [score:1]
Figure 4Western-blot analyses of the functions of miR30-shRNA/nNOS both in vitro (a, b) and in vivo (c, d). [score:1]
A: LVVs-miRLuc-control1; B: LV-SYN-Luc + LV-Tretight-GFP-miR30-shRNA/Luc + LV-mCMV/GfaABC [1]D-tTA. [score:1]
To construct the LV-Tretight-GFP-miR30-shRNA/nNOS shuttle vector, we replaced the Luc shRNA sequence in the LV-Tretight-GFP-miR30-shRNA/Luc shuttle vector with the nNOS shRNA. [score:1]
Figure 2Analyses of the functions of miR30-shRNA/Luc in vitro. [score:1]
A': LVVs-miRLuc-control2; B': LV-GfaABC [1]D-Luc + LV-Tretight-GFP-miR30-shRNA/Luc + LV-mCMV/SYN-tTA. [score:1]
To generate the LV-Tretight-GFP-miR30-shRNA/Luc shuttle vector, we excised the Tretight fragment containing the modified Tet-responsive promoter from pTRE-Tight-DsRed2 (Clontech) and inserted it into the pTYF-SW Linker and cloned, into the obtained vector, PCR product of GFP-miR30-shRNA/Luc cassette from pPRIME-CMV-GFP-FF3 (kindly provided by F. Stegmeier, Harvard Medical School) downstream of Tretight promoter. [score:1]
Our constructs, following the design of Stegmeir et al. used flanking and loop sequences from an endogenous miR30 [37]. [score:1]
Analyses of the functions of miR30-shRNA/Luc in vitro. [score:1]
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4
[+] score: 73
It might occur at the stage of disease initiation: compared with normal Wistar rat, varied copy number of mir-30b and mir-30d in GK might result in altered expression level at some specific developmental stages and at some specific tissues, and the altered expression of mir-30b and mir-30d might then lead to dysfunction of some specific targets, contributing to the development of T2D. [score:10]
We then mapped these microRNA targets to KEGG pathways, and found that 5(2), 12(6), 10(4), 14(12), 4(5) and 1(3) targets of mir-30b(mir-30d) belonged to the pathways of “type II diabetes (04930)”, “Type I diabetes (04940)”, “pancreatic cancer (05212)”, “insulin signaling (04910)”, “PPAR signaling (03320)” and “maturity onset diabetes of the young (04950)”, respectively (Table 4). [score:5]
Since rno-mir-30b was processed to two mature forms, rno-miR-30b-3p and rno-miR-30b-5p, their targets were combined for further analysis; and it was the same with rno-mir-30d, where the targets of rno-miR-30d and rno-miR-30d* were merged. [score:5]
In addition to the aforementioned study of the expression of mir-30d, there were several other expression profiling reports suggesting the involvement of mir-30 family in diabetes or adipogenesis [47]– [49]. [score:5]
It turned out that 39 and 35 targets of mir-30b and mir-30d occurred in this T2D gene list respectively, and were both significantly overrepresented (p = 0.000273 and 0.00152, detailed targets listed in Table 3), supporting the hypothesis of mir-30b and mir-30d's involvement in T2D. [score:5]
Among them, Pparg and Akt2 (targets of mir-30b), Hnf1b, Hnf4a, and Lmna (targets of mir-30d), are well-known genes implicated in T2D or insulin resistance. [score:5]
We re-analyzed a public microRNA expression dataset GSE13920, currently the only one microRNA profiling in GK and Wistar rats [43], and found that the expression levels of mir-30b/30d in muscle cells were strikingly different between normal rat and T2D rat (Figure S2). [score:5]
To further elucidate the putative roles of mir-30b/30d, we looked at their predicted targets using MicroCosm [39]. [score:3]
microRNA Predicted targets rno-mir-30b Aire, Akt2 *, Bud13, Cblb, Cdc123, Eif4e, Elf1, Fgb, Gcg, Hdac3, Irf4, Kcnj5, Klrg1, Mapk8, Med14, Mgea5, Mttp, Neurod1, Nfkb1, Nmu, Parl, Pbx1, Pfkl, Pik3r2, Pparg *, Ppargc1b, Prkce, Prmt2, Rapgef4, Rpa2, Rrad, Serpine1, Slc2a10, Socs1, Srebf1, Tlr4, Ubl5, Ucp2, Wdr42a rno-mir-30d Ace, Cblb, Cdh15, Cp, Cyb5r4, Egfr, Foxo1, Hdac3, Hnf1b *, Hnf4a *, Inpp5k, Irf4, Lgr5, Lmna *, Neurod1, Nfkb2, Nfkbia, Nr1i3, Nr4a1, Parl, Pbx1, Pik3r2, Ppargc1b, Ppp1r3d, Prkar2b, Ptf1a, Rbp4, Rrad, Sell, Sirt1, Slc2a10, Socs1, Sorcs1, Srebf1, Tlr4 *Well-known genes implicated in T2D or insulin resistance. [score:3]
Figure S2 Expression levels of mir-30b/30d in the muscle of GK and Wistar Rat. [score:3]
Targets of rno-mir-30b and rno-mir-30d in T2D-related genes. [score:3]
As for the microRNA expression dataset GSE13920, we simply looked at the mean signal intensities after removing mean background noise for each probe of mir-30b and mir-30d. [score:3]
Table S10 Pathway mapping and enrichment of the targets of rno-mir-30b. [score:3]
The targets of rno-mir-30b and rno-mir-30d involved in diabetes-related pathways. [score:3]
Taken together, there were 1868 and 1776 targets for rno-mir-30b and rno-mir-30d, respectively. [score:3]
The down-regulation of Zfat in muscles is consistent with that of mir-30b and mir-30d, that is, all of them are inconsistent with the CNV gain, suggesting further investigations are still needed to confirm these results and to unveil detailed mechanisms. [score:2]
0014077.g002 Figure 2The microRNA rno-mir-30b and rno-mir-30d located in T2D QTLs. [score:1]
These results provided extra evidence of a role for mir-30b/30d in diabetes pathogenesis. [score:1]
We proposed that the altered copy number of mir-30b and mir-30d in GK rats could contribute to the pathogenesis of T2D. [score:1]
We noticed that there was a protein-coding gene named Zfat which is located at the same gain CNVR as mir-30b and mir-30d are positioned in. [score:1]
The microRNA rno-mir-30b and rno-mir-30d located in T2D QTLs. [score:1]
By comparing the genomic positions of known rat microRNA genes with those of GK/Wistar CNVRs, we found that rno-mir-30b and rno-mir-30d were simultaneously covered by a “gain” region on chromosome 7 in all three samples (Table S9) within a region of only 3.8 Kb. [score:1]
A non-redundant set of CNV regions with the total length of about 36 Mb was identified, including several novel T2D susceptibility loci involving 16 protein-coding genes (Il18r1, Cyp4a3, Sult2a1, Sult2a2, Sult2al1, Nos2, Pstpip1, Ugt2b, Uxs1, RT1-A1, RT1-A3, RT1-Db1, RT1-N1, RT1-N3, RT1-O, and RT1-S2) and two microRNA genes (rno-mir-30b and rno-mir-30d). [score:1]
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5
[+] score: 62
Other miRNAs from this paper: rno-mir-30c-1, rno-mir-30e, rno-mir-30d, rno-mir-30a, rno-mir-30c-2
Our experiments revealed that expression of the miR-30 family was down-regulated in cardiomyocytes of rats from the TAAC group, and that miR-30a expression decreased in hypertrophic cardiomyocytes that had been treated with Ang II. [score:8]
Up-regulation of Autophagy and Down-regulation of miR-30 in Rats with TAAC-Induced Cardiac Hypertrophy. [score:7]
The results of our study indicate that Ang II excessively up-regulates cardiomyocyte autophagy by decreasing miR-30 expression, and that this excessive autophagy promotes the development of myocardial hypertrophy. [score:7]
Taken together, these results provide strong evidence that autophagy mediates the development of myocardial hypertrophy in cardiomyocytes: a down-regulation of miR-30 induced by Ang II leads to excessive autophagy in cardiomyocytes, thereby promoting myocardial hypertrophy. [score:5]
A study by Duisters et al. [10] found that miR-30 family members were significantly down-regulated in mouse hypertrophic hearts and in cardiac biopsies from patients with LVH. [score:4]
The miR-30 family is associated with the development of tumors and other diseases (of the nervous, genital, circulatory, alimentary, and respiratory systems), as well as adipogenesis, cellular senescence, drug metabolism and cell differentiation [16]– [31]. [score:4]
Bioinformatics software predicts that miR-30a may regulate the expression of beclin-1. The function of the miR-30 family is similar to that of other microRNAs. [score:4]
Down-regulation of miR-30 leads to myocardial hypertrophy. [score:4]
Consistent with this, the expression level of miR-30 in the plasma of peripheral blood was elevated in patients with left ventricular hypertrophy (LVH). [score:3]
Autophagy and miR-30 expression in rats after TAAC surgery. [score:3]
circulating miR-30 expression in rats from the TAAC group. [score:3]
It was thus of interest to investigate whether the down-regulation of miR-30 might mediate Ang II -induced myocardial hypertrophy. [score:2]
miR-30-regulated Autophagy in Cardiomyocytes. [score:2]
The expression of miR-30a, miR-30b and miR-30c was significantly lower in rats from the TAAC group, compared with those in the Sham group (Figure 3D). [score:2]
Relationship between the circulating miR-30 level and ventricular wall thickness. [score:1]
Downre-gulation of miR-30 Leads to Myocardial Hypertrophy. [score:1]
Use of plasma miR-30 levels for the diagnosis of LVH reached statistical significance (P = 0.039, Figure 12B). [score:1]
Circulating Levels of miR-30 Increased in Rats Following TAAC Surgery, and in Patients with LVH. [score:1]
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6
[+] score: 62
Here we confirmed that Mtdh represents a target of mi-R30s in DN, and that the expression of all five miR-30 family members is downregulated in the glomeruli form streptozotocin -induced diabetic rats and HG -induced MPC5 cells. [score:8]
Mtdh protein expression was shown to be increased as well after the treatment with the miR-30 inhibitors (Figure 6e), whereas miR-30 mimics significantly reduced Mtdh expression in HG -induced MPC5 cells (Figure 6f). [score:7]
To assess the effects of miR-30s on the expression of Mtdh, we transiently transfected MPC5 cells with miR-30 inhibitors, synthetic miRNA mimics, or their NCs. [score:5]
Furthermore, miR-30 inhibitors significantly increased the expression of Bax and cleaved caspase 3 (Figure 7c). [score:5]
The obtained results demonstrated that miR-30a, -30b, -30c, -30d, and -30e mimics can significantly inhibit the luciferase activity of the wild-type Mtdh 3′-UTR reporter, but not that of the NC, and that this inhibition was reduced when the mutant reporter, with mutated miR-30 -binding site, was used (Figures 5d–h). [score:5]
Transient transfections with siRNAs, Mdth overexpression vector, miR-30 inhibitors, and miR-30 mimics. [score:5]
These cells were transfected with Mtdh siRNA (50 nM; GenePharma, Shanghai, China) or the overexpression (500 ng per well, GenePharma) the mixture of the mimics or inhibitors (RiboBio, Guangzhou, China) of all five miR-30 family members at the final concentrations of 50 nM, using Lipofectamine 2000 (Invitrogen) for 6 h in OPTI-MEM (Gibco BRL), according to the manufacturers' instructions. [score:5]
Mtdh represents a direct target of the members of miR-30 family. [score:4]
Mtdh mRNA level was shown to be significantly increased following the treatment with miR-30 inhibitors (Figure 6c), whereas miR-30s mimics led to a considerable reduction of Mtdh expression induced by HG (Figure 6d), compared with the corresponding NC treatment groups. [score:4]
Therefore, we studied miR-30 expression in the DN glomeruli and HG -induced MPC5 cells. [score:3]
Afterward, OPTI-MEM was replaced with the complete medium containing 1% FBS, and treated with HG for 48 h after the transfection with siRNAs or mimics, whereas the cells treated with miR-30 inhibitors were not treated with HG. [score:3]
MPC5 were transfected with miR-30 inhibitors, mimics, or the respective NCs. [score:3]
analysis demonstrated that the transfection of cells with miR-30 inhibitors significantly increased the percentage of apoptotic cells compared with the NC group (Figure 7a). [score:2]
[44] The 3′-UTR of Mtdh containing putative miR-30 -binding sites was amplified and cloned into PmiR-RB-REPORT dual-luciferase reporter vector (RiboBio). [score:1]
The treatment with miR-30 mimics considerably decreased HG -induced increase in the levels of these proteins (Figure 7d). [score:1]
Conversely, miR-30 mimics considerably reduced the rate of MPC5 apoptosis induced by HG (Figure 7b). [score:1]
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7
[+] score: 58
miRNA chip analysis suggested that expression of rno-miR-344b-3p and rno-miR-30b-3p is enhanced in the renal tissue of rats with adriamycin -induced nephropathy and that triptolide treatment can reverse this upregulation in the expression of rno-miR-344b-3p and rno-miR-30b-3p. [score:8]
These results indicated the expression of rno-miR-344b-3p, rno-miR-195-3p, rno-miR-30b-3p, and rno-miR-34a-5p was significantly upregulated in rats with adriamycin -induced nephropathy, whereas triptolide treatment could reverse the elevated expression of rno-miR-344b-3p and rno-miR-30b-3p to normal levels. [score:8]
Members of the miRNA-30 family are highly expressed in the kidneys of humans and rats [44] and changes in their expression may result in glomerular disease [45]. [score:7]
Treatment with triptolide enhanced expression of five miRNAs (rno-miR-146b-5p, rno-miR-20b-5p, rno-miR-142-3p, rno-miR-223-3p, and rno-miR-21-5p), while that of five other miRNAs (rno-miR-668, rno-miR-203-3p, rno-miR-382-5p, rno-miR-344b-3p, and rno-miR-30b-3p) was significantly downregulated (Tables 3 and 4, and Figure 8). [score:6]
Among them, rno-miR-344b-3p and rno-miR-30b-3p were highly expressed in the mo del group but poorly expressed in the triptolide group. [score:5]
We found that expression of rno-miR-344b-3p and rno-miR-30b-3p in the mo del group was upregulated compared to that observed in the normal group (P < 0.01). [score:5]
In conclusion, triptolide significantly attenuated podocyte injury in rats with adriamycin -induced nephropathy by regulating the expression of miRNA-344-3p and miRNA-30b-3p. [score:4]
We had reasons to believe that expression of rno-miR-344b-3p and rno-miR-30b-3p may play an important role in the protective action of triptolide toward podocytes. [score:3]
It demonstrates that miRNA-344-3p and miRNA-30b-3p might be potential therapeutic targets in the treatment of CKD. [score:3]
Rno-miR-344b-3p and rno-miR-30b-3p were selected as the most differentially expressed miRNAs. [score:3]
Chip analysis showed that, compared to that observed in the normal group, 19 miRNAs were significantly upregulated (rno-miR-344b-3p, rno-miR-195-3p, rno-miR-30b-3p, rno-miR-34a-5p, etc. ) [score:3]
We observed that expression of rno-miR-344b-3p and rno-miR-30b-3p in renal tissues from the mo del group rats was enhanced compared to that observed in the control group. [score:2]
The sequences of miRNA-30b-3p and miRNA-344b-3p were obtained from RiboBio. [score:1]
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8
[+] score: 56
The antagomirs designed to inhibit the expression of endogenous miR-30 members and Antagomir Negative Control were obtained from Ribobio. [score:5]
HWJMSC-EVs Deliver and Restore the Expression of miR-30 in Injured Rat Kidney. [score:3]
In rat kidneys, enforced DRP1 expression and activation were seen in antagomir -treated EVs group, especially in miR-30b/c/d cotreated EVs group (Figure 3(a)). [score:3]
Mitochondrial Apoptotic Pathways Are Inhibited by EVs-Derived miR-30. [score:3]
Quantitative reverse transcriptase polymerase chain reaction (qRT-PCR) showed that IRI caused lower expression of miR-30b, miR-30c, and miR-30d (miR-30a and miR-30e did not exist in rat kidney) and EVs treatment entirely reversed the reduction (Figure 2(a)). [score:3]
Our data demonstrate that miR-30b/c/d reduced in renal tubular cells during IRI and hWJMSCs-EVs could increase the expression of miR-30b/c/d in injured tubular cells both in vitro and in vivo. [score:3]
EVs treatment abrogated the injury and miRNA antagomir did not block this effect in miR-30b/c/d single inhibited group. [score:3]
Meanwhile, antagomir -treated EVs group revealed lower miR-30 expression as well as the vehicle group (Figure 2(c)). [score:3]
We demonstrated that hWJMSC-EVs may ameliorate acute renal IRI by inhibition of mitochondrial fission via miR-30. [score:3]
We next explored the miR-30 expression of rat kidney during IRI in vivo. [score:3]
Given that miR-30 has been reported to regulate mitochondrial fission through the DRP1 pathway on cardiomyocytes [20], we hypothesized that human Wharton Jelly MSCs (hWJMSCs) derived EVs may be involved in the modulation of mitochondrial fission via miR-30, thereby protecting kidney from IRI. [score:2]
To understand how hWJMSC-EVs exert effects on mitochondrial fission, we test whether EVs-derived miR-30 family plays a crucial role in regulating mitochondrial fission through DRP1. [score:2]
EVs-Derived miR-30 Members Regulate Mitochondrial Fission through DRP1. [score:2]
To further explore the mechanism of miR-30 reversion, we used specific miR-30 antagomir to treat MSCs. [score:1]
As we expected, miR-30 antagomir mitigated this effect, especially in miR-30b/c/d antagomir cotreated group. [score:1]
In addition, the mature sequence of human miR-30b/c/d was the same as the rats'. [score:1]
The miR-30 family is involved in several cellular processes, including cardiomyocytes exposed to oxidative stress or ischemia injury and apoptosis of type II alveolar epithelial cells [20, 32, 33]. [score:1]
Here we have identified a miR-30-related antiapoptotic pathway involving DRP1 and mitochondria, which may be one of the mechanisms by which hWJMSC-EVs alleviate renal ischemia reperfusion injury. [score:1]
These data suggested a role of miR-30b/c/d in EVs treatment of IRI. [score:1]
The absence of miR-30 in EVs canceled the miR-30 restoration effects in normal EVs treatment group in vitro. [score:1]
Then, we treated hWJMSCs with miR-30 antagomir. [score:1]
Data showed that miR-30b/c/d were, respectively, absent in EVs derived from MSCs (Figure 2(b)). [score:1]
The sequence of miR-30b antagomir is 5′-AGCUGAGUGUAGGAUGUUUACA-3′; miR-30c antagomir is 5′-GCUGAGAGUGUAGGAUGUUUACA-3′; miR-30d antagomir is 5′-CUUCCAGUCGGGGAUGUUUAGA-3′. [score:1]
The levels of miR-30 family members analyzed by qRT-PCR were normalized to that of U6. [score:1]
S1 MiR-30b/c/d levels in renal tubular epithelial cells in different experimental conditions, including normal, vehicle, EVs and miR-30b/c/d antagomir treated EVs group. [score:1]
We used at least six rats for each group: (1) sham (n = 6); (2) vehicle (n = 6); (3) EVs (n = 6); (4) EVs + antagomir control (n = 6); (5) EVs + antagomir miR-30b (n = 6); (6) EVs + antagomir miR-30c (n = 6); (7) EVs + antagomir miR-30d (n = 6); (8) EVs + antagomir miR-30b/c/d (n = 6). [score:1]
Taken together, it appears that EVs-derived miR-30 can block the mitochondrial apoptotic pathways. [score:1]
Our research reveals links among EVs, miR-30, and DRP1 in the apoptotic program of the kidney. [score:1]
Our results suggest that modulation of miR-30 from EVs may represent a therapeutic approach to treat apoptosis-related renal ischemia reperfusion injury. [score:1]
Our data showed that hWJMSC-EVs could enhance miR-30b/c/d of renal tubular cells and mitigate the activation of DRP1 and mitochondrial fragmentation which leads to antiapoptotic effects. [score:1]
The absence of miR-30 in EVs canceled the miR-30 restoration effects in normal EVs treatment group. [score:1]
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9
[+] score: 55
Interestingly, we discovered that the expression levels of miR-30a, miR-30b, miR-30c, miR-30d and miR-30e were markedly inhibited by cisplatin exposure, especially that of miR-30b, miR-30c and miR-30e as the inhibition was significantly different from that on day 1 of cisplatin injection (Figure 1j). [score:7]
Furthermore, we also demonstrated that miR-30a-e expression was markedly inhibited in HK-2 (Figure 2g) and NRK-52E (Figure 2h) cells exposed to cisplatin, further confirming the observation in renal tissue in Figure 1. As shown on Figures 1 and 2, miR-30b and miR-30c were expressed stronger than miR-30a, miR-30d and miR-30e in renal tubular cells and tissues. [score:7]
By comparing the upregulated genes in the cisplatin -induced kidney injury mo dels, we chose putative genes, including Adrb1, Bnip3L, Hspa5 and MAP3K12, as possible target genes of miR-30 s as they were in the intersection of both database queries (Figure 4a). [score:6]
To elucidate the target genes of miR-30 in cisplatin -induced cell apoptosis, we used bioinformatics tools to predict potential potent target genes. [score:5]
23, 24 Moreover, we detected the expression of the miR-30 family in renal tissue and found that miR-30c was the highest expressed miRNA among the five members (Figure 1i). [score:5]
[38] Guo et al. [38] demonstrated that miR-30e, as a member of the miR-30 family, protected against aldosterone -induced podocyte apoptosis and mitochondrial dysfunction by directly targeting Bnip3L. [score:4]
Although the in vivo evidence about the role of miR-30c on cisplatin -induced renal tubular cell apoptosis lacks, our current experimental results in this study are generally consistent with the observation in which podocyte apoptosis induced by either TGF-beta or puromycin aminonucleoside treatment was ameliorated by exogenously expressing miR-30 and aggravated by the knockdown of miR-30. [score:4]
[34] Here we revealed that all of the miR-30 miRNAs, including miR-30a, miR-30b, miR-30c, miR-30d and miR-30e, were downregulated in both renal tubular epithelial cells and HK-2 cells when cell apoptosis in renal tubules was induced by cisplatin exposure (Figures 1 and 2). [score:4]
[36] Roca-Alonso et al. [37] reported that miR-30 overexpression protects cardiac cells from doxorubicin -induced apoptosis. [score:3]
Likewise, we revealed that the expression levels of miR-30b and miR-30c were higher than that of the other three members in HK-2 (Figure 2e) and NRK-52E (Figure 2f) cells. [score:3]
Using bioinformatics tools, we predicted putative genes, including Adrb1, Bnip3L, Hspa5 and MAP3K12, to be the target genes of miR-30. [score:3]
All of these reports and our results reveal that the miR-30 family indeed has a regulatory role in the modulation of the cell cycle and cell apoptosis in a variety of pathophysiological processes. [score:2]
The reason for focusing on this family is that the miR-30 family is the highest abundant miRNA family in renal tubular epithelial cells according to the results of our previous gene microarray. [score:1]
In this study, we focused on the role of the miR-30 family in the protection of renal tubular cells from the injury induced by cisplatin. [score:1]
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10
[+] score: 51
At 2 h, we saw a trend of upregulation of miR-29b in neurons that steadily increased up to 4-fold at 24 h. In contrast, in astrocytes, miR-29b showed a trend of upregulation later, after 6 h and a significant level increase by 2-fold only after 12 h. MiR-30b, miR-107 and miR-137 were uniquely upregulated only in astrocytes at different time-points, starting 6 h after OGD event. [score:10]
While in neurons undergoing OGD conditions, miR-30b, 107 and 137 did not show any expression alterations, these same miRNAs showed a significant expression upregulation in astrocytes when compared to cells in normoxic conditions. [score:7]
Similarly, in accord with our findings, Ren dell and colleagues [35] reported upregulation of miR-21 and miR-30b occurring 24 h after TBI in brain tissue in a rat mo del. [score:4]
MiR-107, miR-30 and miR-137 were upregulated only in astrocytes. [score:4]
A direct comparison of expression levels of all the miRNAs used for our study between neurons and astrocytes undergoing OGD conditions, showed a significant difference at different time-points only for miR-29b, miR-30b, miR-107 and miR-137 (Figure 1). [score:4]
Recently it was reported that members of miR-30 family are involved in myocardial extracellular matrix remo deling targeting connective tissue growth factors that are induced by TGF-β and endothelin [79]. [score:3]
IGF-I did not have an effect on the expression levels of mir-21, mir-30b, mir-107, mir-137, or mir-210 in neurons. [score:3]
We screened the same miRNAs as described above (miR-21, miR-29b, miR-30b, miR-107, miR-137, miR-210) and found that IGF-I significantly decreases the expression of mir-29b in neurons. [score:3]
MiR-30b, miR-107 and miR-137 did not alter their expression levels in neurons. [score:3]
MiR-29b, miR-30b, miR-107 and miR-137 showed a significant difference in their expression levels between neurons and astrocytes undergoing OGD conditions (Figure 1). [score:3]
MiR-30b showed a trend of expression change at 6, 8 and 12 h (p<0.05). [score:2]
J Cereb Blood Flow Metab 79 Duisters RF Tijsen AJ Schroen B Leenders JJ Lentink V 2009 miR-133 and miR-30 regulate connective tissue growth factor: implications for a role of microRNAs in myocardial matrix remo deling. [score:2]
To our knowledge, the role of miR-30 has not been studied in astrocytes. [score:1]
We screened the same miRNAs as described above (miR-21, miR-29b, miR-30b, miR-107, miR-137, miR-210). [score:1]
It is tempting to speculate a role of miR-30 in controlling apoptosis in astrocytes under hypoxic stress conditions and in induction of astrocyte proliferation and reactive gliosis through similar pathways as in cardiomyocytes. [score:1]
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11
[+] score: 48
Balderman et al. showed that BMP2 increased Runx2 expression in vascular smooth muscle cells and promoted calcification through down -regulating miR-30b-5p 31. miR-103-3p, identified as a mechanosensitive and bone abundant miRNA, inhibited the differentiation of osteoblasts by directly targeting Runx2 32 and the proliferation of osteoblasts by targeting Cav1.2 33. [score:11]
The results showed that 14 miRNAs (miR-30a-5p, miR-30e-5p, miR-425-5p, miR-142-3p, miR-191a-3p, miR-215, miR-29b-3p, miR-30b-5p, miR-26a-5p, miR-345-5p, miR-361-5p, miR-185-5p, miR-103-3p) were down-regulated but no miRNA was up-regulated among above three altered miRNAs from microarray in OVX serum by normalizing to miR-25-3p (Fig. 3b). [score:7]
Eguchi et al. reported that miR-30b-5p expression decreased at the late stage of osteogenic induction and Runx2 was predicted as one of its target genes 30. [score:5]
The clinical characteristics of the subjects were shown in Table 1. Among the detected miRNAs, miR-30b-5p showed significant down-regulation in both osteopenic and osteoporotic patients, while miR-103-3p and miR-142-3p were markedly down-regulated only in osteoporotic patients (Fig. 4a). [score:5]
As shown in Fig. 4c, miR-30b-5p, miR-103-3p and miR-142-3p were significantly down-regulated after bedrest, while miR-328-3p had no significant change. [score:4]
Three serum miRNA (miR-103-3p, miR-142-3p and miR-328-3p) were markedly down-regulated only in osteoporotic patients and miR-30b-5p decreased in both osteopenic and osteoporotic patients. [score:4]
And 3 of them (miR-30b-5p, miR-103-3p and 142-3p) were finally confirmed down-regulation in the serum of both OVX rats, postmenopausal osteoporotic patients and bedrest monkeys. [score:4]
After adjusting for age, weight and height, miR-30b-5p, miR-103-3p, miR-142-3p and miR-328-3p were significantly positively correlated with H-BMD (total hip BMD) (r = 0.541, p = 0.001; r = 0.355, p = 0.039; r = 0.650, p < 0.001; r = 0.355, p = 0.039 respectively). [score:1]
To access the potential diagnostic value of miR-30b-5p for bone loss (osteopenia and osteoporosis), and the value of miR-103-3p, miR-142-3p, miR-328-3p for osteoporosis, ROC analysis was conducted and the associated area under the curve (AUC) was used to confirm the diagnostic value of each miRNA. [score:1]
miR-30b-5p and miR-103-3p were two osteogenesis-related miRNAs. [score:1]
We presumed the possible reasons as following: Firstly, miR-30b-5p and miR-103-3p were identified as ostemiRs in osteoblasts and osteocytes 30, while postmenopausal osteoporosis was mainly due to the over-activity of osteoclasts 34. [score:1]
And the ROC analysis (Fig. 4d) showed considerable diagnostic value: 0.926 for miR-30b-5p (95% CI = 0.67–1.00, p < 0.0001), 0.796 for miR-103-3p (95% CI = 0.52–0.96, p = 0.0133), 0.950 for miR-142-3p (95% CI = 0.68–1.00, p < 0.0001). [score:1]
Meanwhile, miR-30b-5p and miR-142-3p were significantly associated with FN-BMD (femur neck BMD) (r = 0.439, p = 0.009; r = 0.489, p = 0.003 respectively) as well. [score:1]
Secondly, it had been shown that bone loss was partly compensated by increased osteobalstogenesis during estrogen deficiency 35. miR-30b-5p and miR-103-3p may involve in these processes. [score:1]
As shown in Fig. 4b, the AUC of miR-30b-5p was 0.793 (95% CI = 0.625–0.909, p = 0.0001), and 0.800 for miR-103-3p (95% CI = 0.607–0.926, p = 0.0004), 0.789 for miR-142-3p (95% CI = 0.599–0.918, p = 0.0023), and 0.874 for miR-328-3p (95% CI = 0.698–0.967, p < 0.0001). [score:1]
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[+] score: 34
miR-30 family was downregulated during pathological hypertrophy to activate calcium signaling, apoptosis and autophagy pathways miR-133b CyclinD, Nelf-A, RhoA, Ccd42 The expression of miR-133 was upregulated during physiological cardiac hypertrophy. [score:9]
It increases cell survival and negatively regulates apoptosis by targeting Bcl2 miR-30 CaMKIIδ, Egfr1, Bcl2 miR-30 was significantly upregulated during physiological hypertrophy. [score:7]
Hence, it is logical to propose that the downregulated expression of miR-30 family in pathological hypertrophy activates calcium signaling, apoptosis and autophagy pathways. [score:6]
angiotensin II induces down-regulation of miR-30 in cardiomyocytes, which in turn promotes myocardial hypertrophy through excessive autophagy [28]. [score:4]
Our data extend these concepts by demonstrating an upregulation of miR-30 family in physiologically hypertrophied rat heart (Fig. 2A, B). [score:4]
Previous studies indicate that angiotensin II induces down-regulation of miR-30 in cardiomyocytes, which in turn promotes myocardial hypertrophy through excessive autophagy [28]. [score:4]
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[+] score: 33
MiR-30 family members are strongly upregulated during adipogenesis in human cells, and inhibition of miR-30 inhibits adipogenesis [12]. [score:8]
In this study, miR-30a, miR-30b, and miR-30c were significantly downregulated in obese mice, and miR-30b was significantly upregulated after LFD feeding. [score:7]
As shown in the Venn diagram in Fig.   7, notably, 23 of the 28 upregulated miRNAs in DIO + LFD mice (mmu-miR-16, mmu-let-7i, mmu-miR-26a, mmu-miR-17, mmu-miR-107, mmu-miR-195, mmu-miR-20a, mmu-miR-25, mmu-miR-15b, mmu-miR-15a, mmu-let-7b, mmu-let-7a, mmu-let-7c, mmu-miR-103, mmu-let-7f, mmu-miR-106a, mmu-miR-106b, mmu-miR-93, mmu-miR-23b, mmu-miR-21, mmu-miR-30b, mmu-miR-221, and mmu-miR-19b) were downregulated in the DIO mice. [score:7]
Notably, 23 circulating miRNAs (mmu-miR-16, mmu-let-7i, mmu-miR-26a, mmu-miR-17, mmu-miR-107, mmu-miR-195, mmu-miR-20a, mmu-miR-25, mmu-miR-15b, mmu-miR-15a, mmu-let-7b, mmu-let-7a, mmu-let-7c, mmu-miR-103, mmu-let-7f, mmu-miR-106a, mmu-miR-106b, mmu-miR-93, mmu-miR-23b, mmu-miR-21, mmu-miR-30b, mmu-miR-221, and mmu-miR-19b) were significantly downregulated in DIO mice but upregulated in DIO + LFD mice. [score:7]
miR-30 family members have also been demonstrated to act as positive regulators of adipocyte differentiation in a human adipose tissue-derived stem cell mo del [35]. [score:2]
Some of the circulating miRNAs identified in this study have also been reported in the adipose tissue of DIO mice or implicated in adipogenic processes [11– 13], including Let-7, miR-103, miR-15, the miR-17-92 cluster (miR-17, miR-20a, and miR-92a), miR-21, miR-221, and miR-30b. [score:1]
The miR-30 family has been found to be important for adipogenesis [12]. [score:1]
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[+] score: 21
These results suggested a correlation between the increased expression levels of miR-101, miR-30b, miR-30c, and miR-30d, as well as the decreased Sox9 expression level. [score:5]
The expression of miR-101, miR-30b, miR-30c, miR-30d and miR-27b was detected (Figure 1D) but miR-1 and miR-30e expression was not (data not shown). [score:5]
However, no negative regulatory effects on Sox9 expression were observed in miR-30b, miR-30c and miR-30d on (Figures 2D and 2E). [score:4]
The increasing expression of miR-101, miR-30b, miR-30c, and miR-30d emerged at different time points after IL-1β treatment (Figure 1D). [score:3]
Six miRNAs (miR-1, miR-101, miR-30b, miR-30c, miR-30d, and miR-30e) were selected to potentially target Sox9 (Figure 1A). [score:3]
However, luciferase activity was not reduced with the mimics of miR-30b, miR-30c, and miR-30d (Figure 2C). [score:1]
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[+] score: 21
Based on functional and pathway analysis and related literature examination, we selected miR-134-5p, miR-207, and miR-465-5p to represent the up-regulated miRNAs, and miR-30b-5p, miR-19a-3p, and miR-130a-3p to represent the down-regulated miRNAs. [score:7]
Among these DEmiRNAs, 6 up- or down-regulated miRNAs were chosen for further analysis, including miR-134-5p, miR-207, miR-465-5p, miR-30b-5p, miR-19a-3p, and miR-130a-3p. [score:4]
In our network, Chst1 (carbohydrate sulfotransferase 1) is regulated by four miRNAs, including miR-30b-5p, miR-19a-3p, miR-130a-3p, and miR-134-5p, while Nrbf2 (nuclear receptor binding factor 2) is regulated by miR-30b-5p, miR-19a-3p, miR-130a-3p, and miR-207. [score:3]
The DEmiRNAs (e. g., miR-134-5p, miR-207, miR-465-5p, miR-30b-5p, miR-19a-3p, and miR-130a-3p) and common target genes, such as Chst1 and Nrbf2, may be strongly associated with the pulmonary inflammation induced by ZnO-NPs. [score:3]
Additionally, in our study, Nrbf2 was regulated by miR-30b-5p, miR-19a-3p, miR-130a-3p, and miR-207. [score:2]
Finally, Scn9a is modulated by miR-30b-5p, miR-130a-3p, miR-134-5p, and miR-465-5p. [score:1]
Chst1 is modulated by four miRNAs, including miR-30b-5p, miR-19a-3p, miR-130a-3p, and miR-134-5p. [score:1]
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[+] score: 21
24-Hour Acute ZT06 Expression 24-Hour Chronic ZT06 Expression 2-Week chronic ZT06 Expression rno-miR-142-5p Over rno-miR-126a-5p Under rno-miR-146a-5p Under rno-miR-150-5p Over rno-miR-30b-5p Under rno-miR-24-3p Under rno-miR-335 Under rno-let-7b-5p Over rno-miR-130a-3p Over rno-miR-15b-5p Over rno-miR-99a-5p Over rno-miR-127-3p Under rno-miR-133a-3p Under rno-miR-10a-5p Over rno-miR-672-5p Over rno-miR-l-3p Under rno-let-7c-5p Over rno-miR-193-3p Over rno-miR-142-5p Under rno-miR-146b-5p Under rno-miR-150-5p Over Of the three ZT06 groups that illustrated differential expression of miRNAs due to CD, emphasis was placed on the two-week chronic ZT06 group due to the differential expression of miRs 146a and 146b, and miR-127 (Figures 5A-5B and 6A). [score:11]
24-Hour Acute ZT06 Expression 24-Hour Chronic ZT06 Expression 2-Week chronic ZT06 Expression rno-miR-142-5p Over rno-miR-126a-5p Under rno-miR-146a-5p Under rno-miR-150-5p Over rno-miR-30b-5p Under rno-miR-24-3p Under rno-miR-335 Under rno-let-7b-5p Over rno-miR-130a-3p Over rno-miR-15b-5p Over rno-miR-99a-5p Over rno-miR-127-3p Under rno-miR-133a-3p Under rno-miR-10a-5p Over rno-miR-672-5p Over rno-miR-l-3p Under rno-let-7c-5p Over rno-miR-193-3p Over rno-miR-142-5p Under rno-miR-146b-5p Under rno-miR-150-5p Over Differentially expressed miRNAs based on Illumina sequencing in all the circadian-disrupted samples and their links to breast cancer development and circadian rhythms. [score:10]
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[+] score: 18
Consistently, in our study of the roles of miR-30 in regulation of autophagy, we observed that only expression of miR-30c showing around 62 % decrease during activation of autophagy under I/R injury conditions in Fig.   2a. [score:4]
The result showed no changes in expression of miR-30 except that decreased in miR-30c (Fig.   2a) suggesting an involvement of miR-30c in neuroprotective effect against spinal cord ischemia-reperfusion injury of H2S. [score:3]
I/R group To explore the mechanisms how H [2]S could attenuate I/R -induced spinal cord injury, we examined the expression of miR-30 profiles by using. [score:3]
Recent study showed that miR-30 could impair autophagic process by targeting multiple genes in the autophagy pathway [27]. [score:3]
OGD group Recent study showed that miR-30 could impair autophagic process by targeting multiple genes in the autophagy pathway [22]. [score:3]
Fig. 2Expression of microRNA30 profiles and autophagy-related protein in rats spinal cord. [score:2]
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[+] score: 14
Disagreements extend to other cell death-related microRNAs that were reported by Liu [6] to demonstrate changes in expression that we were not able to detect (mir-137 and miR-672) or whose expression did not seem to change in the present study (miR-214, miR-30-3p, miR-235-3p, and miR-674-5p). [score:5]
In fact, according to previous studies [17], [18], [19], [21], [22], highly expressed microRNAs in the spinal cord or the CNS, such as miR-125b, miR-29a, miR-30b, and miR-9*, show sustained, high levels of expression before and after injury (see file S1), suggesting an overall preservation of the cell populations in the spinal cord. [score:5]
In agreement with their results, we observed the downregulation of miR-127, miR-181a, miR-411, miR-99a, miR-34a, miR-30b, and miR-30c, which according to Liu [6] should lead to increased inflammation. [score:4]
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[+] score: 11
miRNA expression profiling of lung tissues demonstrated differential expression of seven miRNAs, with downregulation of miR-344a-3p (−2.36-fold change) and upregulation of miR-103 (4.04-fold change), miR-22 (2.72-fold change), miR-30b-5p (1.51-fold change), miR-347 (1.95-fold change), miR-382 (2.82-fold change), and miR-3573-3p (3.32-fold change) (Figures 3A,B). [score:11]
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[+] score: 11
Another recent study suggested that down-regulation of miR-30 family leads to endoplasmic reticulum stress in vascular smooth muscle cells [25] and a similar trend of down-regulation is shown in the case of miR-30d and miR-30e. [score:7]
Previous studies have shown that miR-30 family members negatively regulate osteoblast differentiation [24] and also suggest RUNX2 and SMAD1 are common post-transcriptional targets of miR-30 family. [score:4]
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21
[+] score: 11
miR-99a and miR-30b were confirmed to be the up-regulated miRNAs in ARDS, while miR-126 and miR-26a were confirmed to be down-regulated miRNAs in ARDS (Figure  2). [score:7]
The up-regulated miRNAs included miR-99a, miR-127, miR-128b, miR-135b, miR-30a, and miR-30b. [score:4]
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[+] score: 11
In the mo del group, 17 miRNAs were downregulated, including miR-1, miR-133, miR-29, miR-126, miR-212, miR-499, miR-322, miR-378, and miR-30 family members, whereas the other 18 miRNAs were upregulated, including miR-21, miR-195, miR-155, miR-320, miR-125, miR-199, miR-214, miR-324, and miR-140 family members. [score:7]
Among these differentially expressed miRNAs, miR-1, miR-133, miR-29, miR-126, miR-499, miR-30, miR-21, miR-195, miR-155, miR-199, miR-214, and miR-140 have been reported to be related to MI [25– 36], while the other miRNAs have not been reported directly in MI. [score:4]
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[+] score: 10
The underlying mechanism might be related to the modulation of 18 upregulated and 14 downregulated miRNAs, in particular, miR-20a, miR-145, miR-30, and miR-98. [score:7]
Thus, involution was obtained by miChip analysis for four selected miRNAs that showed either high (miR-145) or low (miR-30) signal intensities, or high (miR-20a) or low (miRNA-98) differential expression values among the three groups. [score:3]
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[+] score: 10
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-26b, hsa-mir-29a, hsa-mir-30a, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-106a, mmu-let-7g, mmu-let-7i, mmu-mir-15b, mmu-mir-29b-1, mmu-mir-30a, mmu-mir-30b, mmu-mir-125a, mmu-mir-125b-2, mmu-mir-130a, mmu-mir-138-2, mmu-mir-181a-2, mmu-mir-182, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-30e, hsa-mir-10a, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-182, hsa-mir-181a-1, mmu-mir-297a-1, mmu-mir-297a-2, mmu-mir-301a, mmu-mir-34c, mmu-mir-34b, mmu-let-7d, mmu-mir-106a, mmu-mir-106b, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-30b, hsa-mir-125b-1, hsa-mir-130a, hsa-mir-138-2, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-138-1, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-15a, mmu-mir-26b, mmu-mir-29a, mmu-mir-29c, mmu-mir-34a, rno-mir-301a, rno-let-7d, rno-mir-344a-1, mmu-mir-344-1, rno-mir-346, mmu-mir-346, rno-mir-352, hsa-mir-181b-2, mmu-mir-10a, mmu-mir-181a-1, mmu-mir-29b-2, mmu-mir-138-1, mmu-mir-181b-1, mmu-mir-181c, mmu-mir-125b-1, hsa-mir-106b, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-34b, hsa-mir-34c, hsa-mir-301a, hsa-mir-30e, hsa-mir-362, mmu-mir-362, hsa-mir-369, hsa-mir-374a, mmu-mir-181b-2, hsa-mir-346, rno-let-7a-1, rno-let-7a-2, rno-let-7b, rno-let-7c-1, rno-let-7c-2, rno-let-7e, rno-let-7f-1, rno-let-7f-2, rno-let-7i, rno-mir-10a, rno-mir-15b, rno-mir-26b, rno-mir-29b-2, rno-mir-29a, rno-mir-29b-1, rno-mir-29c-1, rno-mir-30c-1, rno-mir-30e, rno-mir-30d, rno-mir-30a, rno-mir-30c-2, rno-mir-34b, rno-mir-34c, rno-mir-34a, rno-mir-106b, rno-mir-125a, rno-mir-125b-1, rno-mir-125b-2, rno-mir-130a, rno-mir-138-2, rno-mir-138-1, rno-mir-181c, rno-mir-181a-2, rno-mir-181b-1, rno-mir-181b-2, rno-mir-181a-1, hsa-mir-449a, mmu-mir-449a, rno-mir-449a, mmu-mir-463, mmu-mir-466a, hsa-mir-483, hsa-mir-493, hsa-mir-181d, hsa-mir-499a, hsa-mir-504, mmu-mir-483, rno-mir-483, mmu-mir-369, rno-mir-493, rno-mir-369, rno-mir-374, hsa-mir-579, hsa-mir-582, hsa-mir-615, hsa-mir-652, hsa-mir-449b, rno-mir-499, hsa-mir-767, hsa-mir-449c, hsa-mir-762, mmu-mir-301b, mmu-mir-374b, mmu-mir-762, mmu-mir-344d-3, mmu-mir-344d-1, mmu-mir-673, mmu-mir-344d-2, mmu-mir-449c, mmu-mir-692-1, mmu-mir-692-2, mmu-mir-669b, mmu-mir-499, mmu-mir-652, mmu-mir-615, mmu-mir-804, mmu-mir-181d, mmu-mir-879, mmu-mir-297a-3, mmu-mir-297a-4, mmu-mir-344-2, mmu-mir-466b-1, mmu-mir-466b-2, mmu-mir-466b-3, mmu-mir-466c-1, mmu-mir-466e, mmu-mir-466f-1, mmu-mir-466f-2, mmu-mir-466f-3, mmu-mir-466g, mmu-mir-466h, mmu-mir-493, mmu-mir-504, mmu-mir-466d, mmu-mir-449b, hsa-mir-374b, hsa-mir-301b, rno-mir-466b-1, rno-mir-466b-2, rno-mir-466c, rno-mir-879, mmu-mir-582, rno-mir-181d, rno-mir-182, rno-mir-301b, rno-mir-463, rno-mir-673, rno-mir-652, mmu-mir-466l, mmu-mir-669k, mmu-mir-466i, mmu-mir-669i, mmu-mir-669h, mmu-mir-466f-4, mmu-mir-466k, mmu-mir-466j, mmu-mir-1193, mmu-mir-767, rno-mir-362, rno-mir-504, rno-mir-582, rno-mir-615, mmu-mir-3080, mmu-mir-466m, mmu-mir-466o, mmu-mir-466c-2, mmu-mir-466b-4, mmu-mir-466b-5, mmu-mir-466b-6, mmu-mir-466b-7, mmu-mir-466p, mmu-mir-466n, mmu-mir-344e, mmu-mir-344b, mmu-mir-344c, mmu-mir-344g, mmu-mir-344f, mmu-mir-374c, mmu-mir-466b-8, hsa-mir-466, hsa-mir-1193, rno-mir-449c, rno-mir-344b-2, rno-mir-466d, rno-mir-344a-2, rno-mir-1193, rno-mir-344b-1, hsa-mir-374c, hsa-mir-499b, mmu-mir-466q, mmu-mir-344h-1, mmu-mir-344h-2, mmu-mir-344i, rno-mir-344i, rno-mir-344g, mmu-let-7j, mmu-mir-30f, mmu-let-7k, mmu-mir-692-3, rno-let-7g, rno-mir-15a, rno-mir-762, mmu-mir-466c-3, rno-mir-29c-2, rno-mir-29b-3, rno-mir-344b-3, rno-mir-466b-3, rno-mir-466b-4
Such a situation occurred for miR-26b, miR-30, and miR-374 downregulation, and for miR-34, miR-301, and miR-352 upregulation [121]. [score:7]
These miRNAs (miR-15a, miR-30, miR-182, and miR-804) are involved in cell proliferation, apoptosis, inflammation, epithelial-mesenchymal transition, invasion, oncogene inhibition, and intercellular adhesion. [score:3]
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[+] score: 9
According to this observation, Caruso et al. (2010) showed that, during the onset of pulmonary arterial hypertension (PAH) after hypoxia, there is a reduced Dicer expression leading to miR-22, miR-30, and let-7f down-regulation and, at the same time, to miR-322 and miR-451 up-regulation in two different PAH rat mo dels. [score:9]
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[+] score: 9
Although the mechanisms underlying regulation of glycogene expression remain to be clarified, several studies have reported that micro RNAs [41, 42], such as miR-30b/d targeting both Galnt1 and Galnt7 [43] and epigenetic modifications, contribute to the regulation of glycogene expression in cancer cells and leukocytes [44, 45]. [score:9]
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[+] score: 8
It was found to be targeted by multiple microRNAs in our analysis, including miR-143, miR-30 family members, miR-140, miR-27b, miR-125a-5p, miR-128ab, and miR-342-3p. [score:3]
Among the important genes were Lifr, Acvr1c, and Pparγ which were found to be targeted by microRNAs in our dataset like miR-143, miR-30, miR-140, miR-27b, miR-125a, miR-128ab, miR-342, miR-26ab, miR-181, miR-150, miR-23ab and miR-425. [score:3]
According to our in silico analysis, Ppar γ is likely regulated by microRNAs like let-7 family members, miR-30 family members, miR-27b, miR-23ab, miR-93, miR-25, miR-128ab, miR-320, and miR-135. [score:2]
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[+] score: 8
Other miRNAs from this paper: rno-mir-30c-1, rno-mir-30e, rno-mir-30d, rno-mir-30a, rno-mir-30c-2
In this study, we constructed a PDGFR-β shRNA expression plasmid, in which PDGFR-β shRNA embedded in an miR30 -based context was driven by a CMV promoter. [score:3]
The PDGFR-β shRNA was inserted immediately into the miR30 -based shRNA expression system of the pCMR30 vector (Genechem, Shanghai, China) to generate a pCMV–shRNA–red fluorescent protein (RFP), in which PDGFR-β shRNA was driven by the CMV promoter and RFP was the reporter gene. [score:3]
To generate pCMV–shRNA–LacZ, the fragment containing miR30 -based PDGFR-β shRNA was PCR-cloned into the HindIII site of the pMIR-REPORT β-gal reporter control vector (Ambion, Austin, TX, USA), which supplies the β-gal reporter gene. [score:1]
As a negative control, we generated pCMV–NC–LacZ with miR30 -based PDGFR-β shRNA in pCMV–shRNA–LacZ replaced by negative control RNA. [score:1]
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[+] score: 7
It is noteworthy that miR-1, miR-133, miR-30, miR-208a, miR-208b, mir-499, miR-23a, miR-9 and miR-199a have previously been shown to be functionally involved in cardiovascular diseases such as heart failure and hypertrophy [40], [41], [42], [43], [44], and have been proposed as therapeutic- or disease-related drug targets [45], [46]. [score:7]
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30
[+] score: 6
Liu et al. showed that miR-30b is involved in MGO -induced EMT of peritoneal mesothelial cells in rats; miR-30b directly inhibited bone morphogenetic protein-7 (BMP-7) by binding to its 3′-untranslated region, causing unavailability of BMP-7 that might be the antagonist of TGF- β1 -induced EMT [26]. [score:6]
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31
[+] score: 6
Shen Y. Shen Z. Miao L. Xin X. Lin S. Zhu Y. Guo W. Zhu Y. Z. miRNA-30 family inhibition protects against cardiac ischemic injury by regulating cystathionine-γ-lyase expression Antioxid. [score:6]
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32
[+] score: 6
According to recent studies, miRs regulate cells or tissues exposed to myocardial infarction or ischemia, with reports finding that miR-21 protects hearts from ischemic injury via PDCD4 expression [2], miR-361 transfected into rat hearts causes mitochondrial fission and myocardial ischemic injury [36], and miR-30b protects cardiomyocytes by inhibiting cyclophilin D [3]. [score:6]
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33
[+] score: 5
The altered regulation of miR-30a is also of interest because the miR-30 family is well studied but has not previously been reported as being involved in vascular changes after SAH. [score:2]
Duisters RF, Tijsen AJ, Schroen B, Leenders JJ, Lentink V, van der Made I, et al. miR-133 and miR-30 regulate connective tissue growth factor: implications for a role of microRNAs in myocardial matrix remo deling. [score:2]
The miR-30 family members are known for their role in angiogenesis-related myocardial matrix remo deling via their interaction with connective tissue growth factor [37]. [score:1]
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34
[+] score: 5
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-21, hsa-mir-26b, hsa-mir-27a, hsa-mir-29a, hsa-mir-30a, hsa-mir-33a, hsa-mir-98, hsa-mir-29b-1, hsa-mir-29b-2, mmu-let-7g, mmu-let-7i, mmu-mir-27b, mmu-mir-29b-1, mmu-mir-30a, mmu-mir-30b, mmu-mir-126a, mmu-mir-133a-1, mmu-mir-135a-1, mmu-mir-141, mmu-mir-194-1, mmu-mir-200b, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-30e, hsa-mir-203a, hsa-mir-211, hsa-mir-218-1, hsa-mir-218-2, hsa-mir-200b, mmu-mir-300, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-27b, hsa-mir-30b, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-135a-1, hsa-mir-135a-2, hsa-mir-141, hsa-mir-194-1, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, mmu-mir-200a, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-21a, mmu-mir-26b, mmu-mir-29a, mmu-mir-29c, mmu-mir-27a, mmu-mir-98, mmu-mir-326, rno-mir-326, rno-let-7d, rno-mir-343, rno-mir-135b, mmu-mir-135b, hsa-mir-200c, mmu-mir-200c, mmu-mir-218-1, mmu-mir-218-2, mmu-mir-33, mmu-mir-211, mmu-mir-29b-2, mmu-mir-135a-2, hsa-mir-194-2, mmu-mir-194-2, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-30e, hsa-mir-326, hsa-mir-135b, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, rno-let-7a-1, rno-let-7a-2, rno-let-7b, rno-let-7c-1, rno-let-7c-2, rno-let-7e, rno-let-7f-1, rno-let-7f-2, rno-let-7i, rno-mir-21, rno-mir-26b, rno-mir-27b, rno-mir-27a, rno-mir-29b-2, rno-mir-29a, rno-mir-29b-1, rno-mir-29c-1, rno-mir-30c-1, rno-mir-30e, rno-mir-30d, rno-mir-30a, rno-mir-30c-2, rno-mir-33, rno-mir-98, rno-mir-126a, rno-mir-133a, rno-mir-135a, rno-mir-141, rno-mir-194-1, rno-mir-194-2, rno-mir-200c, rno-mir-200a, rno-mir-200b, rno-mir-203a, rno-mir-211, rno-mir-218a-2, rno-mir-218a-1, rno-mir-300, hsa-mir-429, mmu-mir-429, rno-mir-429, hsa-mir-485, hsa-mir-511, hsa-mir-532, mmu-mir-532, rno-mir-133b, mmu-mir-485, rno-mir-485, hsa-mir-33b, mmu-mir-702, mmu-mir-343, mmu-mir-466b-1, mmu-mir-466b-2, mmu-mir-466b-3, hsa-mir-300, mmu-mir-511, rno-mir-466b-1, rno-mir-466b-2, rno-mir-532, rno-mir-511, mmu-mir-466b-4, mmu-mir-466b-5, mmu-mir-466b-6, mmu-mir-466b-7, mmu-mir-466b-8, hsa-mir-3120, rno-mir-203b, rno-mir-3557, rno-mir-218b, rno-mir-3569, rno-mir-133c, rno-mir-702, rno-mir-3120, hsa-mir-203b, mmu-mir-344i, rno-mir-344i, rno-mir-6316, mmu-mir-133c, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, mmu-mir-30f, mmu-let-7k, mmu-mir-3569, rno-let-7g, rno-mir-29c-2, rno-mir-29b-3, rno-mir-466b-3, rno-mir-466b-4, mmu-mir-203b
We used TargetScan and miRanda database queries to obtain miRNAs, which had higher targeting combined with N4bp2, namely, miR-200, miR-429, miR-29 and miR-30. [score:5]
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35
[+] score: 5
For instance, we observed a decrease in the levels of 5 miRNA with predicted target sites in the Foxa1 3′UTR (miR-106b, miR-194, miR-30c, miR-30b-5p and miR-20a) along with increased Foxa1 mRNA expression on methamphetamine exposure. [score:5]
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36
[+] score: 5
There were no significant changes in the expression of miR-15, miR-30, and miR-133a between healthy subjects and patients with burn injury. [score:3]
MiR-195, let-7e, miR-15, miR-133a, and miR-30 did not show any significant difference between burn rats and sham rats (Figure 1A) (P>0.05). [score:1]
MiR-15, miR-133a, and miR-30 also had P [CT] > 0.75. [score:1]
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37
[+] score: 4
Other miRNAs from this paper: rno-mir-30c-1, rno-mir-30e, rno-mir-30d, rno-mir-30a, rno-mir-30c-2
Previous studies have demonstrated that angiotensin II could induce the down-regulation of miR-30 [41], increase mitochondria oxidative stress [42], thereby causing myocardium autophagy, which indicated that RAS activation could result in the cellular autophagy. [score:4]
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38
[+] score: 4
Gain- and loss-of-function miRNA studies and luciferase reporter assays reported that miR-204 [24], miR-133a [25], and miR-30b-c [26] inhibited the osteogenic differentiation of mice VSMCs and human coronary artery smooth muscle cells (SMCs) during β-glycerophosphate -induced calcification through the targeting of RUNX2. [score:4]
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39
[+] score: 4
miR-30 regulates mitochondrial fission through targeting p53 and the dynamin-related protein-1 pathway. [score:4]
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40
[+] score: 4
Other miRNAs from this paper: rno-mir-30c-1, rno-mir-30e, rno-mir-30d, rno-mir-30a, rno-mir-30c-2
As previously reported [14], short hairpin RNAs targeting firefly luciferase (accession number M15077, non-mammalian control, luciferase shRNA), rat VEGF [164] (accession number AF260425, VEGF [164] shRNA) and rat VEGFA (accession number NM_031836, VEGF-A shRNA) were embedded into a microRNA (miR-30) context. [score:3]
The miR-30/shRNAs were cloned into a lentiviral transfer vector under transcriptional control of a CD44 promoter (pFmCD44.1 GW), with green fluorescent protein (GFP) as a reporter gene. [score:1]
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41
[+] score: 4
Pan et al. reported that miR-30-regulated autophagy mediates angiotensin II -induced myocardial hypertrophy [44], which implies that there exists a complicated network for mediating autophagy that has yet to be determined. [score:2]
It should be noted that the miR-352-IGF2R pathway may not be the only mechanism for regulating autophagy during collateral vessel growth because additional miRNAs involved in autophagy were identified, such as, miR-30. [score:2]
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42
[+] score: 4
As shown in Table 2, we found increased expression of liver specific miRNAs in transdifferentiated hepatocytes, including miR-122a, miR-21, miR-22, miR-182, miR-29 and miR-30. [score:3]
By computer software prediction, HNF-4 binding sites are also present in the 5′ upstream regions of miR-21, miR-30b and miR-30d. [score:1]
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43
[+] score: 4
PE + miR30 inhibitor. [score:3]
PE + miR30 mimics, [&&]p < 0.01 vs. [score:1]
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44
[+] score: 3
Other miRNAs from this paper: rno-mir-30c-1, rno-mir-30e, rno-mir-30d, rno-mir-30a, rno-mir-30c-2
Column 4 is a similar co transfection with another shRNA vector based on the mir-30 system that contains the same shRNA targeting sequence as the shRNA shown in column 3 experiments. [score:3]
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45
[+] score: 3
We extracted 60 different human miRNAs that co-occur with this target gene from 79 PubMed abstracts, and some of them (e. g. hsa-let-7a, hsa-miR-30b, hsa-miR-183) are consistent with microarray -based results discussed by Shalgi et al. [44]. [score:3]
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46
[+] score: 3
Six candidate miRNAs that are predicted to target caspase-3 (let-7, miR-138, miR-30b, miR-129, miR-203, and miR-219-5p) and have an aggregate Pct greater than 0.2 were selected (Fig.   1c). [score:3]
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47
[+] score: 3
Other miRNAs from this paper: rno-mir-30c-1, rno-mir-30e, rno-mir-30d, rno-mir-30a, rno-mir-30c-2
The template “miRNA30‐like” DNA oligonucleotides targeting two positions of NR1 mRNAs (shRNAmir1 and shRNAmir2) were ligated into the XhoI/ MluI sites in the pGIPZ‐shRNAmir vector (Open Biosystems). [score:3]
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48
[+] score: 3
MicroRNA-30b -mediated regulation of catalase expression in human ARPE-19 cells. [score:3]
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49
[+] score: 3
The luciferase values were further normalized to the average luciferase value obtained after transfecting a panel of microRNAs not predicted to target the rat Arc 3′UTR (rno-miR-370, rno-miR-150, rno-miR-342, rno-miR-30b, rno-miR-105, rno-miR-145 and rno-miR-9). [score:3]
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50
[+] score: 3
Specifically, some studies have focused on the roles of miRNAs in the protective effects of fish oil or omega-3 PUFAs against metabolic syndrome and found that the intake of fish oil or DHA/EPA can modify the expression of miR-30b and miR-378 [49], miR-33a and miR-122 [50], miR-107 [51], miR-192, and miR-30c [52]. [score:3]
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[+] score: 2
The target miRNAs (and corresponding assay numbers) were: rno-miR-23a (000399), rno-miR-26b (000407), rno-miR-30-5p (000420), rno-miR-101b (002531), rno-miR-125b-5p (000449), rno-miR-379 (001138) and rno-miR-431 (001979). [score:2]
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52
[+] score: 2
We designed and cloned into the pcPURhU6 vector the hairpin-type RNAs with si-6 sequence (pcPURhU6 si-6) with the 19-21 base pair (bp) stems and with various loops: (1) pcPURhU6 si-6 (21 bp)-miR26, (2) si-6 (19 bp) with 9-nt UUCAAGAGA loop [28], (3) si-6 (21 bp) with 9-nt UUCAAGAGA loop, (4) si-6 (21 bp) with 10-nt CUUCCUGUCA (loop from miRNA23), and (5) si-6 (21 bp) with 19-nt UAGUGAAGCCACAGAUGUA (loop from miRNA30) (see Figure 3). [score:1]
Constructs 4 and 5 with miRNA-origin loops miRNA23 and miRNA30, respectively, demonstrated moderate silencing activity, lowering BACE1 mRNA by 27% and 38%, respectively. [score:1]
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[+] score: 2
Moreover, the fine coordination of activity of the transmembrane receptor smoothened by the miR-30 family allows the correct specification and differentiation of distinct muscle cell types during zebrafish embryonic development 41. [score:2]
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54
[+] score: 2
Duisters R. F. Tijsen A. J. Schroen B. Leenders J. J. Lentink V. van der Made I. Herias V. van Leeuwen R. E. Schellings M. W. Barenbrug P. miR-133 and miR-30 regulate connective tissue growth factor: Implications for a role of micrornas in myocardial matrix remo deling Circ. [score:2]
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55
[+] score: 2
The amiRNAs represent a type of shRNAs in which a siRNA sequence is embedded into a native microRNA scaffold [30], most commonly into that of miR-30 [30], [31] or miR-155 [32], [33]. [score:1]
We confirmed that the silencing efficiency of amiR155-PLBr used here was comparable to that using a miR-30 scaffold (data not shown). [score:1]
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56
[+] score: 2
5 miR-503* −5.7 miR-376c* −4.0 miR-215 −1.4 miR-30b* −1.3 miR-29c* −1.2All groups except the BDL and HFD groups showed necrosis and inflammation. [score:1]
5 miR-503* −5.7 miR-376c* −4.0 miR-215 −1.4 miR-30b* −1.3 miR-29c* −1.2 All groups except the BDL and HFD groups showed necrosis and inflammation. [score:1]
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57
[+] score: 2
Duisters R. F. Tijsen A. J. Schroen B. Leenders J. J. Lentink V. van der Made I. Herias V. van Leeuwen R. E. Schellings M. W. Barenbrug P. miR-133 and miR-30 regulate connective tissue growth factor: Implications for a role of microRNAs in myocardial matrix remo deling Circ. [score:2]
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58
[+] score: 1
All short hairpin RNAs (shRNAs) were generated using a mir-30 -based design method, which has been previously described [25]. [score:1]
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59
[+] score: 1
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-17, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-29a, hsa-mir-30a, hsa-mir-31, hsa-mir-32, hsa-mir-33a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-106a, mmu-let-7g, mmu-let-7i, mmu-mir-27b, mmu-mir-30a, mmu-mir-30b, mmu-mir-126a, mmu-mir-9-2, mmu-mir-135a-1, mmu-mir-137, mmu-mir-140, mmu-mir-150, mmu-mir-155, mmu-mir-24-1, mmu-mir-193a, mmu-mir-194-1, mmu-mir-204, mmu-mir-205, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-143, mmu-mir-30e, hsa-mir-34a, hsa-mir-204, hsa-mir-205, hsa-mir-222, mmu-let-7d, mmu-mir-106a, mmu-mir-106b, hsa-let-7g, hsa-let-7i, hsa-mir-27b, hsa-mir-30b, hsa-mir-135a-1, hsa-mir-135a-2, hsa-mir-137, hsa-mir-140, hsa-mir-143, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-126, hsa-mir-150, hsa-mir-193a, hsa-mir-194-1, mmu-mir-19b-2, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, mmu-mir-200a, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-15a, mmu-mir-23a, mmu-mir-24-2, mmu-mir-29a, mmu-mir-31, mmu-mir-92a-2, mmu-mir-34a, rno-mir-322-1, mmu-mir-322, rno-let-7d, rno-mir-329, mmu-mir-329, rno-mir-140, rno-mir-350-1, mmu-mir-350, hsa-mir-200c, hsa-mir-155, mmu-mir-17, mmu-mir-25, mmu-mir-32, mmu-mir-200c, mmu-mir-33, mmu-mir-222, mmu-mir-135a-2, mmu-mir-19b-1, mmu-mir-92a-1, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-7b, hsa-mir-194-2, mmu-mir-194-2, hsa-mir-106b, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-30e, hsa-mir-375, mmu-mir-375, mmu-mir-133b, hsa-mir-133b, rno-let-7a-1, rno-let-7a-2, rno-let-7b, rno-let-7c-1, rno-let-7c-2, rno-let-7e, rno-let-7f-1, rno-let-7f-2, rno-let-7i, rno-mir-7b, rno-mir-9a-1, rno-mir-9a-3, rno-mir-9a-2, rno-mir-17-1, rno-mir-19b-1, rno-mir-19b-2, rno-mir-23a, rno-mir-24-1, rno-mir-24-2, rno-mir-25, rno-mir-27b, rno-mir-29a, rno-mir-30c-1, rno-mir-30e, rno-mir-30d, rno-mir-30a, rno-mir-30c-2, rno-mir-31a, rno-mir-32, rno-mir-33, rno-mir-34a, rno-mir-92a-1, rno-mir-92a-2, rno-mir-106b, rno-mir-126a, rno-mir-135a, rno-mir-137, rno-mir-143, rno-mir-150, rno-mir-193a, rno-mir-194-1, rno-mir-194-2, rno-mir-200c, rno-mir-200a, rno-mir-204, rno-mir-205, rno-mir-222, hsa-mir-196b, mmu-mir-196b, rno-mir-196b-1, mmu-mir-410, hsa-mir-329-1, hsa-mir-329-2, mmu-mir-470, hsa-mir-410, hsa-mir-486-1, hsa-mir-499a, rno-mir-133b, mmu-mir-486a, hsa-mir-33b, rno-mir-499, mmu-mir-499, mmu-mir-467d, hsa-mir-891a, hsa-mir-892a, hsa-mir-890, hsa-mir-891b, hsa-mir-888, hsa-mir-892b, rno-mir-17-2, rno-mir-375, rno-mir-410, mmu-mir-486b, rno-mir-31b, rno-mir-9b-3, rno-mir-9b-1, rno-mir-126b, rno-mir-9b-2, hsa-mir-499b, mmu-let-7j, mmu-mir-30f, mmu-let-7k, hsa-mir-486-2, mmu-mir-126b, rno-mir-155, rno-let-7g, rno-mir-15a, rno-mir-196b-2, rno-mir-322-2, rno-mir-350-2, rno-mir-486, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
Interestingly, among the conserved miRNAs found in all epididymal regions, we identified 8/14 and 4/7 members of the let-7 family (let-7a—let-7f, let-7i) and miR-30 (miR-30a— miR-30d) family, respectively. [score:1]
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60
[+] score: 1
MiR-30 was shown to induce apoptosis [32] and regulate cell motility by influencing the extracellular matrix remo deling process [33– 35]. [score:1]
[1 to 20 of 1 sentences]
61
[+] score: 1
Other miRNAs from this paper: rno-mir-30d
A set of T2D -associated CNV regions with the total length of about 36 Mb, including several novel T2D susceptibility loci which contain 16 protein-coding genes (Il18r1, Cyp4a3, Sult2a1, Sult2a2, Sult2al1, Nos2, Pstpip1, Ugt2b, Uxs1, RT1-A1, RT1-A3, RT1-Db1, RT1-N1, RT1-N3, RT1-O, and RT1-S2) and two microRNA genes (rno-mir-30b and rno-mir-30d), were identified [36]. [score:1]
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62
[+] score: 1
Lentiviral vectors encoding miR-20a or a control sequence within a common miR-30 backbone have been previously described [16]. [score:1]
[1 to 20 of 1 sentences]
63
[+] score: 1
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-16-1, hsa-mir-17, hsa-mir-21, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-30a, hsa-mir-31, hsa-mir-96, hsa-mir-99a, hsa-mir-16-2, hsa-mir-30c-2, hsa-mir-30d, hsa-mir-182, hsa-mir-183, hsa-mir-211, hsa-mir-217, hsa-mir-218-1, hsa-mir-218-2, hsa-mir-221, hsa-mir-222, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-23b, hsa-mir-30b, hsa-mir-125b-1, hsa-mir-132, hsa-mir-143, hsa-mir-145, hsa-mir-191, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-184, hsa-mir-190a, hsa-mir-195, rno-mir-322-1, rno-let-7d, rno-mir-335, rno-mir-342, rno-mir-135b, hsa-mir-30c-1, hsa-mir-299, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-379, hsa-mir-382, hsa-mir-342, hsa-mir-135b, hsa-mir-335, rno-let-7a-1, rno-let-7a-2, rno-let-7b, rno-let-7c-1, rno-let-7c-2, rno-let-7e, rno-let-7f-1, rno-let-7f-2, rno-let-7i, rno-mir-15b, rno-mir-16, rno-mir-17-1, rno-mir-21, rno-mir-23a, rno-mir-23b, rno-mir-24-1, rno-mir-24-2, rno-mir-25, rno-mir-26a, rno-mir-26b, rno-mir-30c-1, rno-mir-30e, rno-mir-30d, rno-mir-30a, rno-mir-30c-2, rno-mir-31a, rno-mir-96, rno-mir-99a, rno-mir-125a, rno-mir-125b-1, rno-mir-125b-2, rno-mir-126a, rno-mir-132, rno-mir-143, rno-mir-145, rno-mir-183, rno-mir-184, rno-mir-190a-1, rno-mir-191a, rno-mir-195, rno-mir-211, rno-mir-217, rno-mir-218a-2, rno-mir-218a-1, rno-mir-221, rno-mir-222, rno-mir-299a, hsa-mir-384, hsa-mir-20b, hsa-mir-409, hsa-mir-412, hsa-mir-489, hsa-mir-494, rno-mir-489, rno-mir-412, rno-mir-543, rno-mir-542-1, rno-mir-379, rno-mir-494, rno-mir-382, rno-mir-409a, rno-mir-20b, hsa-mir-542, hsa-mir-770, hsa-mir-190b, hsa-mir-543, rno-mir-466c, rno-mir-17-2, rno-mir-182, rno-mir-190b, rno-mir-384, rno-mir-673, rno-mir-674, rno-mir-770, rno-mir-31b, rno-mir-191b, rno-mir-299b, rno-mir-218b, rno-mir-126b, rno-mir-409b, rno-let-7g, rno-mir-190a-2, rno-mir-322-2, rno-mir-542-2, rno-mir-542-3
These include rno-miR-195, rno-miR-125a-5p, rno-let-7a, rno-miR-16, rno-miR-30b-5p, rno-let-7c, rno-let-7b, rno-miR-125b-5p, rno-miR-221, rno-miR-222, rno-miR-26a, rno-miR-322, rno-miR-23a, rno-miR-191, rno-miR-30 family, rno-miR-21, rno-miR-126, rno-miR-23b, rno-miR-145 and rno-miR-494. [score:1]
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