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39 publications mentioning rno-mir-23b

Open access articles that are associated with the species Rattus norvegicus and mention the gene name mir-23b. 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: 282
The miR-23b mimics, mimics negative control (mimics control), inhibitor, inhibitor negative control (inhibitor control), the small interfering RNA targeting Smad3 (siSmad3) and control-siRNA (siCtrl), the Smad3 overexpression plasmid (pcDNA-Smad3) and negative control (Ctrl) were purchased from Genepharma Inc (Shanghai, China). [score:11]
Compared with miR-23b mimics and inhibitor negative controls, transfection of miR-23b mimics led to a dramatic increase of miR-23b, and transfection of miR-23b inhibitor suppressed endogenous miR-23b expression (Fig 3A). [score:8]
Thyrotropin Regulates Thyroid Cell Proliferation by Up-Regulating miR-23b and miR-29b that Target SMAD3. [score:7]
To well underlying molecular mechanism of miR-23b suppresses the proliferation and migration of heat-denatured fibroblasts, bioinformatic analysis of three publicly available algorithms (PicTar, TargetScan and miRBase) was performed to explore the target gene of miR-23b. [score:7]
Our results indicate that the recovery of heat-denatured dermis and fibroblasts depends on the upregulation of Smad3, resulting from the downregulation of miR-23b. [score:7]
In this study, it was found that miR-23 directly targets and regulates Smad3 expression in denatured dermis and heat-denatured fibroblasts. [score:7]
In addition, Smad3 protein was upregulated with heat-denatured dermis, which was in agreement with the downregulation of miR-23b in denatured dermis. [score:7]
These results suggested that up-and down-regulation of Smad3 mimicked the effect of decreasing and increasing miR-23b expression in heat-denatured fibroblasts. [score:6]
These results clearly demonstrate that suppression of miR-23 promotes the proliferation and migration of heat-denatured fibroblasts, suggesting that downregulation of miR-23b might be required for the recovery of heat-denatured dermis and fibroblasts. [score:6]
Our study showed that miR-23b downregulation resulting from transfection with inhibitor increased the levels of Notch1 and TGF-β. [score:6]
In addition, downregulation of miR-23 could increase the expression of Notch1 and TGF-β. [score:6]
Very interestingly, a recent miRNA microarray analysis between denatured dermis and normal skin of patients revealed distinct expression profiles of mRNAs, in which miR-23b was found to be significantly downregulated in denatured dermis [12]. [score:6]
Western blotting analysis of cleaved Notch1 and TGF-β expression in fibroblasts after transfection with miR-23b mimics or inhibitor. [score:5]
Further mechanistic investigation found that miR-23 directly targets and regulates Smad3 expression in denatured dermis and heat-denatured fibroblasts. [score:5]
It was found that transfection with miR-23b inhibitor increased the levels of Notch1 and TGF-β, while miR-23b mimics decreased the expression of Notch1, but not TGF-β (Fig 8A). [score:5]
0131867.g003 Fig 3 (A) miR-23b expression level was examined by quantitative RT-PCR after transfection with mimics and inhibitor. [score:5]
In this study, it was demonstrated that miR-23b is dynamically expressed during the recovery of heat-denatured dermis and fibroblasts, and inhibition of miR-23b results in enhanced proliferation and migration of heat-denatured fibroblasts. [score:5]
0131867.g008 Fig 8 Western blotting analysis of cleaved Notch1 and TGF-β expression in fibroblasts after transfection with miR-23b mimics or inhibitor. [score:5]
0131867.g005 Fig 5 (A) Western blotting analysis of Smad3 expression after transfection of miR-23b mimics, inhibitor and control in fibroblasts. [score:5]
However, the physiological consequence of miR-23b downregulation is largely unknown. [score:4]
In summary, our study demonstrates that miR-23b plays important roles in the regulation of the survival and growth of denatured dermis and suggests that miR-23b -mediated control of Smad3 expression may be fundamental for skin regeneration after severe burns. [score:4]
Smad3 is a direct target of miR-23b. [score:4]
miR-23b was downregulated in denatured dermis and heat-denatured fibroblasts. [score:4]
Thus, the downregulation of miR-23 contributes to the survival and proliferation of fibroblasts in the dermis after severe burns. [score:4]
In addition, our previous study showed that miR-23b is downregulated in the denatured dermis of deep burn patients [10]. [score:4]
Downregulation of miR-23b promotes the proliferation and migration of heat-denatured fibroblasts. [score:4]
Our findings suggest that downregulation of miR-23b contributes to the recovery of denatured dermis, which may be valuable for treatment of skin burns. [score:4]
These results demonstrate that miR-23b binds directly to the 3’UTR of Smad3 to repress its expression in heat-denatured fibroblasts. [score:4]
However, the molecular mechanism and physiologic functions of the downregulation of miR-23b in the recovery of denatured dermis during wound healing is unknown. [score:4]
Compared with that of normal skin, miR-23b expression significantly decreased in denatured dermis, with the greatest inhibitory rate of 81% after three days, but then gradually increased three days post-burn. [score:4]
Li et al. found that miR-23b was significantly upregulated in keloid fibroblasts and may partially contribute to the etiology of keloids by affecting several signaling pathways [28]. [score:4]
To validate that Smad3 is a direct target of miR-23b, Smad3 luciferase reporters were constructed with wild-type and mutated 3’UTR of Smad3. [score:4]
Downregulation of miR-23b dramatically promoted the proliferation and migration of heat-denatured fibroblasts. [score:4]
To test whether Smad3 can be regulated by miR-23b, the protein level of Smad3 in heat-denatured human fibroblasts transfected with miR-23b mimics or inhibitor was determined by Western blotting. [score:4]
Histological examination of denatured dermis and the expression of miR-23b in denatured dermis. [score:3]
To explore the expression of miR-23b during the recovery of denatured dermis, the skin tissues of the deep partial-thickness burn rats were collected at different time points after burn creation and stained with hematoxylin and eosin (HE). [score:3]
Expression of miR-23b in normal skin and heat-denatured dermis. [score:3]
However, the mechanism of the suppression of miR-23b in the dermis after burns remains to be determined. [score:3]
Our data demonstrates that targeting Smad3 is one of the mechanisms by which miR-23b controls the activity of many intracellular transduction pathways. [score:3]
Expression of miR-23b in heat-denatured human fibroblasts. [score:3]
In thyroid cells, miR-23b and miR-29b can promote cell growth by targeting Smad3 [27]. [score:3]
Morphological change of heat-denatured fibroblasts and the expression level of miR-23b in heat-denatured fibroblasts. [score:3]
The 3’untranslated region (3’UTR) of Smad3 containing the miR-23b binding sites was amplified by PCR from human genomic DNA. [score:3]
To test whether the Notch1 and TGF-β signaling pathways are involved in miR-23b-modulated fibroblasts growth and migration after heat damage, the protein levels of TGF-β and cleaved Notch1 in heat-denatured human fibroblasts transfected with miR-23b mimics or inhibitor were determined by Western blotting. [score:3]
Subsequent analyses demonstrated that Smad3 was a direct and functional target of miR-23b in heat-denatured fibroblasts, which was validated by the dual luciferase reporter assay. [score:3]
The expression of miR-23b in denatured dermis and heat-denatured fibroblasts was detected by quantitative real-time polymerase chain reaction (RT-PCR). [score:3]
Several studies suggest that miR-23b may function as either a tumor suppressor gene [18] or oncogene [19] and play important roles in cell proliferation, migration and differentiation [20– 23], depending on the type of cancer. [score:3]
The effects of miR-23b on cell proliferation and migration of heat-denatured fibroblasts were assessed by transient transfection of miR-23b mimics and inhibitor. [score:3]
miR-23b has been reported to promote tolerogenic properties of dendritic cells via inhibition of the Notch1/NF-κB signaling pathways [24]. [score:3]
The results showed that miR-23b mimics dramatically decreased the protein level of Smad3, while miR-23b inhibitor increased the Smad3 protein level in heat-denatured human fibroblasts (Fig 5A). [score:3]
Our results demonstrate that miR-23b is decreased in the early stages of the recovery of heat-denatured dermis and fibroblasts and inhibition of miR-23b results in enhanced proliferation and migration of heat-denatured fibroblasts. [score:3]
Similar to denatured dermis, heat-denatured fibroblasts also demonstrated a time -dependent change in miR-23b expression. [score:3]
MiR-23 directly targets Smad3. [score:3]
Furthermore, in agreement with the decreased expression of miR-23b (Fig 1B), immunohistochemistry of denatured dermis showed that the staining of Smad3 in denatured dermis three days after burning was much stronger than that in normal skin (Fig 5B). [score:3]
As shown in Fig 1B, miR-23b expression demonstrated a dynamic alteration during the recovery of denatured dermis. [score:3]
These reporters were co -transfected with miR-23b mimics or inhibitor into heat-denatured human fibroblasts. [score:3]
In this study, we assessed the potential role of miRNA-23b (miR-23b) in the regulation of cell proliferation and migration of heat-denatured fibroblasts and identified the underlying mechanism. [score:2]
Regulation of the Notch1 and TGF-β signaling pathways by miR-23b. [score:2]
As shown in Fig 5D, the luciferase activity was significantly decreased or increased compared to either mutant or empty controls when co -transfected with miR-23b mimics or inhibitor, respectively. [score:2]
Taken together, our results clearly demonstrate that miR-23b is dynamically regulated during the recovery of both denatured dermis and heat-denatured human fibroblasts, suggesting an essential role for miR-23b during wound healing. [score:2]
Moreover, miR-23b cluster miRNA was diminished during the termination of liver regeneration and regulated the growth and differentiation of liver stem cells through TGF-β/bone morphogenetic protein signaling [25, 26]. [score:2]
After 48 h, the proliferation of cells transfected with miR-23b inhibitor significantly increased compared with cells transfected with scramble mimics or untreated cells. [score:2]
Next, fibroblasts were subjected to heat damage 12 h after transfection of miR-23b mimics or inhibitor and cell proliferation was assessed by CCK-8 assay at 24, 48 and 72 h after transfection. [score:2]
MiR-23b suppressed the proliferation of heat-denatured fibroblasts. [score:2]
However, the molecular mechanism of the regulation of these various signal transduction pathways by miR-23b, especially Notch1/NF-κB and TGF-β/bone morphogenetic protein signaling pathways, remains elusive. [score:2]
These findings suggest that the Notch1 and TGF-β signaling pathways might also be involved in the regulation of cell growth and migration of denatured dermis and fibroblasts by miR-23b. [score:2]
MiR-23b suppressed migration of heat-denatured fibroblasts. [score:2]
To investigate the biological function of miR-23b in heat-denatured fibroblasts, human fibroblasts were transfected with miR-23b mimics to increase the endogenous level of miR-23b, or miR-23b inhibitor to decrease the level of miR-23b. [score:1]
Modulation of the Notch1 and TGF-β signaling pathways by miR-23b and Smad3. [score:1]
The target gene of miR-23b and the downstream pathway were further investigated. [score:1]
showed that the migration capacity of cells transfected with miR-23b inhibitor was dramatically increased compared with the scramble and control group and the migration capacity of cells transfected with miR-23b mimics was dramatically decreased compared with the scramble and control group cells (Fig 4). [score:1]
The expression of miR-23b during the recovery of denatured dermis was evaluated. [score:1]
In this study, the roles of miR-23b in denatured dermis were explored. [score:1]
To explore the physiologic functions of miR-23b during the recovery of denatured dermis, a mo del of human heat-denatured fibroblasts was established following the methods described by Li et al. [13]. [score:1]
The wild-type 3’UTR of Smad3 as well as mutant 3’UTR with nucleotide substitutions in the putative binding sites corresponding to the seed sequence of miR-23b were inserted into the psiCHECK-2 vector immediately downstream of the stop codon of luciferase to develop psiCHECK2-Smad3-3’UTR and psiCHECK-Smad3-mut-3’UTR, respectively. [score:1]
The miRNA sequence-specific reverse transcription (RT)-PCR for miR-23b and endogenous control U6 was performed using Hairpin-it miRNAs qPCR quantitation kit and U6 snRNA real-time PCR normalization kit (GenePharma, Shanghai, China). [score:1]
Next, the expression of miR-23b in the denatured dermis was measured at different recovery time points after burn creation (1, 3, 5, and 7 days) by RT-PCR. [score:1]
revealed complementarity between Smad3 3’UTR and miR-23b. [score:1]
qRT-PCR was performed to validate the level of miR-23b after transfection. [score:1]
These findings suggest that miR-23b promotes the growth and migration of denatured dermis and fibroblasts by activing Notch1 and TGF-β signaling pathways. [score:1]
In addition, miR-23b modulated denatured dermis by activating the Notch1 and TGF-β signaling pathways. [score:1]
The miR-23b levels in heat-denatured fibroblasts at different time points following heat damage were determined by RT-PCR. [score:1]
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[+] score: 165
Other miRNAs from this paper: rno-mir-23a
There is growing evidence indicating that miRNAs play an important role in toxicogenomics, disease etiology, and the effect of toxicants 26. miR-23b has been reported as a small RNA with a broad regulatory role, for example, it is known to regulate gene expression and anti-oxidant or pro-oxidant pathways, and it plays a role in tumor development 27. miR-23b inhibited the generation of reactive oxygen species by inhibiting the expression of NOX4, a member of the NADPH oxidase family 28, it was also found to trigger cancer-promoting effects by inhibiting the expression of apoptosis antigen 1 (FAS) and the tumor suppression gene, phosphatase and tensin homolog (PTEN), in lymphoma and kidney cancer 29 30. [score:20]
Pretreatment of miR-23b mimic significantly inhibited CYP3A1 expression in H4IIE cells treated with BDE47, while the miR-23b inhibitor enhanced expression (Fig. 5A). [score:9]
Using bioinformatics software, miR-23a and miR-23b could target the nucleic acid sequence of rat CYP3A1 but only miR-23b was affected by BDE47, and miR-23b could directly bind to the 3′-UTR region of CYP3A1 and inhibit the expression of CYP3A1. [score:8]
These results clearly illustrate that miR-23b acts as a miRNA that targets CYP3A1 mRNA and it plays an important role in the BDE47 -induced expression and activity of CYP3A by targeting transcriptional regulation. [score:8]
Correspondingly, the miR-23b inhibitor decreased the intracellular miR-23b level (Fig. 4C), and up-regulated CYP3A1 expression (Fig. 4E). [score:8]
miR-23b not only regulated BDE47 -induced expression of CYP3A1 and corresponding cytotoxicity of H4IIE cells, but it also regulated the expression and activity of CYP3A1, as well as the oxidative metabolism of BDE47 in rats. [score:7]
The miR-23b mimic increased the intracellular miR-23b level (Fig. 4B), and down-regulated the expression of CYP3A1(Fig. 4D). [score:6]
H4IIE cells were treated with mock (M), miR-23b mimic or negative control (NC) for 24 h. (C) Effects of miR-23b inhibitor on the expression of miR-23b. [score:5]
H4IIE cells were treated with 20 or 40 μM BDE47 for 24 h after miR-23b inhibitor pretreatment for 24 h. The data is expressed as the mean ± SD of three independent experiments with triplicate samples. [score:5]
H4IIE cells were treated with mock, miR-23b inhibitor, or negative control for 24 h. The data is expressed as the mean ± SD of three independent experiments with triplicate samples. [score:5]
miR-23b mimic, miR-23b inhibitor, and miRNA mimic and inhibitor negative control (NC) were purchased from RiBoBio (Guangzhou, China). [score:5]
Blockage of miR-23b by Lv-anti-miR-23b significantly increased the expression and activity of CYP3A1 in liver microsomes of rats treated with BDE47, and it also increased oxidative metabolites of BDE47 (3-OH-BDE47, 4-OH-BDE47, and 4′-OH-BDE47) in the serum, further revealing the important role of miR-23b in BDE47 -induced expression and activity of CYP3A1. [score:5]
How to cite this article: Sun, Z. et al. BDE47 induces rat CYP3A1 by targeting the transcriptional regulation of miR-23b. [score:4]
These data suggest that miR-23b potentially regulates the expression of rat CYP3A1 and human CYP3A4. [score:4]
Regulation of miR-23b on BDE47 -induced CYP3A1 expression and cytotoxicity in H4IIE cells. [score:4]
As expected, LV-anti-miR-23b alone not only significantly decreased miR-23b levels, but also increased the expression and activity of CYP3A1 in rat liver. [score:3]
BDE47 treatment alone showed similar results, and those findings were further augmented in the co-treatment of BDE47 and LV-anti-miR-23b in rats, which exemplified the important role of miR-23b in BDE47 -induced expression and activity of CYP3A1 (Fig. 6A–C). [score:3]
Effects of miR-23b on the expression and activity of CYP3A1 in rats treated with BDE47. [score:3]
H4IIE cells were treated with 20 or 40 μM BDE47 for 24 h after miR-23b mimic pretreatment for 24 h. (C) Effects of miR-23b inhibitor on BDE47 -induced cytotoxicity. [score:3]
H4IIE cells were treated with 20 μM BDE47 for 24 h after miR-23b mimic or miR-23b inhibitor pretreatment for 24 h. (B) Effects of miR-23b mimic on BDE47 -induced cytotoxicity. [score:3]
Effects of miR-23b on CYP3A expression. [score:3]
Effects of miR-23b on BDE47 -induced CYP3A1 expression and activity in rats. [score:3]
Moreover, the miR-23b mimic reversed and the miR-23b inhibitor aggravated the decrease in the viability of H4IIE cells treated with BDE47 (Fig. 5B,C), providing evidence that BDE47 -mediated miR-23b induced CYP3A1, and subsequent cytotoxicity of H4IIE cells. [score:3]
Effects of miR-23b on the expression of CYP3A1 in H4IIE cells. [score:3]
To further determine the role of miR-23b in the function of CYP3A1 in the liver, rats received a caudal vein injection of LV-anti-miR-23b or LV-NC, which were chosen for their effects on miR-23b and CYP3A1 expression in H4IIE cells (Fig. S3). [score:3]
In the present study, miR-23b was found to inhibit the metabolic activation of BDE47 in H4IIE cells, which was further confirmed in rats treated with BDE47. [score:3]
However, the effect of miR-23b on the expression of CYP enzymes is still unknown. [score:3]
Effects of miR-23b on BDE47 -induced expression of CYP3A1 and cytotoxicity in H4IIE cells. [score:3]
To validate these findings, the pGL3p/3′UTR plasmid was co -transfected with miR-23b mimic or a miR-23b inhibitor into H4IIE cells. [score:3]
Effects of BDE47 on miR-23 expression. [score:3]
[##] P < 0.01, compared with the negative control for miR-23b mimics or inhibitor. [score:2]
These results suggest that miR-23b contributed to the metabolism of BDE47 through the regulation of CYP3A1. [score:2]
However, miR-23a was not affected by BDE47 (Fig. 3A,B), but miR-23b significantly decreased in H4IIE cells treated with BDE47 (10 μM or 20 μM) and rat liver tissue treated with 0.001 mg/kg BDE47, generated from our previous study 14, indicating that miR-23b instead of miR-23a is involved in the induction of CYP3A1 by BDE47 (Fig. 3C,D). [score:1]
However, the recognition sites of miR-23b exist in the CDS regions of CYP3A4 mRNA, the mechanism and effects need to be further elucidated. [score:1]
Various fragments containing the miR-23b MRE were inserted at the Xba I site downstream of the luciferase gene in the pGL3-promoter vector. [score:1]
As shown in Table S1, high complementary pairing sites of miR-23 (miR-23a and miR-23b) existed in CYP3A1 3′-UTR/CDS sequences. [score:1]
Thirty rats were randomly divided into three groups and were given an intravenous injection of 500 μL PBS solution, Lentiviral -negative control (LV-NC), or LV-anti-miR-23b. [score:1]
Based on in vitro and in vivo experiments, we first investigated the role of miR-23b in the BDE47 -induced expression and activity of CYP3A1. [score:1]
Bioinformatics analysis identified a potential miR-23b recognition element (MRE23b) in rat CYP3A1 and human CYP3A4 mRNA. [score:1]
Luciferase reporters with CYP3A1 CDS or 3′-UTR were used in H4IIE cells co -transfected with miR-23b mimics or miR-control. [score:1]
For human CYP3A4, as predicted for the complementary pairing sites of miR-23b and CYP3A4 (Fig. S2A), the reporter activities of the pGL3p/ CYP3A4 CDS (+80–+1588), particularly CDS (+450–+750), (+1150–+1400), and (+1490–+1710) (Fig. S2C), were significantly lower than that of the control plasmid (Fig. S2B, C), which was further confirmed by the results for the mutants of their corresponding CDS regions (Fig. S2D). [score:1]
The luciferase assay revealed that endogenous and exogenous miR-23b negatively regulated the activity through MRE23b. [score:1]
Thirty rats were randomly divided into three groups and were given an intravenous injection of 500 μL PBS solution, Lentiviral -negative control (LV-NC, 5 × 10 [7 ]TU), or Lentiviral-anti-miR-23b (LV-anti-miR-23b, 5 × 10 [7 ]TU). [score:1]
To investigate whether miR-23b is functional in the regulation of CYP3A expression, luciferase assays were performed using H4IIE cells and HepG2 cells. [score:1]
These results suggest that miR-23b functionally recognizes the 3′-UTR region on the rat CYP3A1 mRNA. [score:1]
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[+] score: 161
The miR-23b/27b cluster suppresses HSC activation by directly binding gremlin1 mRNA 3′-UTR and downregulates gremlin1 expression to correct the imbalance of TGF-β and BMP-7 signal transduction (Figure 6). [score:9]
Accordingly, we conclude that the miR-23b/27b cluster inhibits HSC activation by directly binding gremlin1 mRNA and downregulating its expression. [score:9]
Downregulation of gremlin1 expression by the miR-23b/27b cluster leads to decreased expression of hepatic fibrosis-related factors. [score:8]
To examine this theory, we investigated the mechanisms underlying gremlin1 expression and HSC activation, specifically, the effects of gremlin1 downregulation on HSC activation and hepatic fibrosis in vivo and the capacity of the miR-23b/27b cluster to suppress gremlin1 expression. [score:8]
Notably, the miR-23b/27b cluster downregulates gremlin1 expression via binding to its 3′-UTR region, leading to suppression of HSC activation. [score:8]
These data suggest that miR-23b-3p, miR-27b-5p and miR-27b-3p bind to target sequences in the 3′-UTR and downregulate gremlin1 expression. [score:8]
However, it remains to be established whether the miR-23b/27b cluster has the capacity to inhibit gremlin1 expression via negative post-transcriptional regulation, and as a result, suppress HSC activation during hepatic fibrogenesis. [score:8]
Schematic representation of suppression of HSC activation through downregulation of gremlin1 expression by the miR-23b/27b. [score:8]
The miR-23b/27b cluster suppresses HSC activation through downregulating gremlin1 expression. [score:8]
Binding of miR-27b and miR-23b to gremlin1 mRNA 3′-UTR led to a marked decrease in gremlin1 expression as well as inhibition of α-SMA, collagen Iα1, Iα2 and TGF-β expression in HSCs. [score:7]
Figure 5(A– C) Expression levels of hepatic fibrosis-related factors, including α-SMA, TGF-β, collagen Iα1 and collagen Iα2, were critically assessed via western blot of the proteins from HSC-T6 cells transfected with miR-23b/27b mimics, inhibitors, negative control or inhibitor control, respectively. [score:7]
As the miR-23b/27b cluster appears to directly inhibit gremlin1 expression, we rigorously analyzed its effects on HSC activation. [score:6]
The contribution of the miR-23b/27b cluster in downregulation of gremlin1 expression was further confirmed via western blot. [score:6]
For this purpose, we identified miR-27b and miR-23b were evidently involved in downregulation of gremlin1 expression in HSCs. [score:6]
The miR-23b/27b cluster downregulates gremlin1 expression. [score:6]
Endogenous gremlin1 expression in HSC-T6 cells was downregulated in the presence of miR-23b-3p, miR-27b-5p and miR-27b-3p mimics (p < 0.05), but not the miR-23b-5p mimic (p > 0.05) (Figure 4E, 4F). [score:6]
Luciferase activity of cells transfected with pMIR-Luc-3′-UTR followed by treatment with the miR-23b-5p mimic was significantly decreased (p < 0.01), compared to those treated with the negative control mimics, but no significant increase (p > 0.05) was evident after treatment with its inhibitors, with no obvious changes (p > 0.05) between inhibitor and inhibitor control treatments (Figure 4D). [score:6]
Firstly, treatment with the miR-23b-3p, miR-27b-5p or miR-27b-3p mimics, compared to the corresponding inhibitors, led to downregulation of α-SMA in HSC-T6 cells (p < 0.05) (Figure 5A, 5C). [score:5]
These findings clearly suggest that the miR-23b/27b cluster suppresses activation of HSCs and inhibits collagen synthesis. [score:5]
Recent studies have demonstrated that the miR-23b/27b cluster directly downregulates epidermal growth factor receptor and hepatocyte growth factor receptor [36]. [score:5]
One member of the miR-23b/27b cluster, miR-27b, has the potential to inhibit fibrosis in pulmonary cells through targeting gremlin1 [18]. [score:5]
In this study, we hypothesized that gremlin1 stimulates HSC activation and is downregulated by the miR-23b/27b cluster, leading to alleviation of hepatic fibrosis via rectifying the imbalance between TGF-β and BMP-7 signaling. [score:4]
The miR-23b/27b cluster, a prognostic marker in renal cell carcinoma [20], has shown to suppress the metastatic phenotype of castration-resistant prostate cancer cells [21]. [score:3]
Data from the current study highlight the utility of the miR-23b/27b cluster as a novel target for manipulation in clinical therapy of hepatic fibrosis. [score:3]
The mimic sequences of miR-23a/27a, miR-23b/27b and inhibitors of miR-23b/27b were got from the miRBase (http://www. [score:3]
The results showed a significant decrease in luciferase activity of cells transfected with pMIR-Luc-3′-UTR followed by treatment with the miR-23b-3p (p < 0.01), miR-27b-5p (p < 0.01) and miR-27b-3p (p < 0.01) mimics, compared to cells treated with the negative control mimic or their inhibitors. [score:2]
Accordingly, the two clusters of miR-23a/27a and miR-23b/27b were selected for subsequent experiments. [score:1]
of collagen Iα1 and Iα2 revealed a significant decrease in collagen Iα1 and Iα2 in HSC-T6 cells treated with the miR-27b-5p (p < 0.05) or miR-27b-3p (p < 0.01) mimic, but not those treated with the miR-23b-3p mimic (p > 0.05) (Figure 5A, 5C). [score:1]
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[+] score: 32
A 12-week treatment with RDE increased the expression of rno-miR-20b-5p and rno-miR-23b-3p and decreased the expression of rno-miR-191a-5p in alveolar bone (Figure 3a–d), which could result in the down-regulation of Jak1, STAT3, Il6r and up-regulation of Il6. [score:11]
RDE increased the expression of rno-miR-20b-5p and rno-miR-23b-3p in alveolar bone after 12 weeks of treatment (Figure 3a–d), which could result in the down-regulation of target gene expression, including Tgfbr2/Bmpr2, Smad3/4/5, Bcl2. [score:10]
This inhibitory effect of RDE occurred via the regulation of miRNA expression (rno-miR-20b-5p, rno-miR-23b-3p and rno-miR-191a-5p) and lead to a down-regulation of high rate of bone turnover resulted from ovariectomy. [score:9]
Name Primers U6F: 5′-GCTTCGGCAGCACATATACTAAAAT-3′ R: 5′-CGCTTCACGAATTTGCGTGTCAT-3′ rno-miR-500-3pGSP: 5′-GGAAGGCACCTGGGCAAG-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-499-3pGSP: 5′-GGGGAACATCACAGCAAGTC-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-214-3pGSP: 5′-GGGGACAGCAGGCACAGAC-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-20b-5pGSP: 5′-GGGGCAAAGTGCTCATAGTG-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-877GSP: 5′-GGGGAAGTAGAGGAGATGGC-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-451-5pGSP: 5′-GGGGGAAACCGTTACCATTAC-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-3577GSP: 5′-GGGTTCTGTCCCTCTTGGC-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-370-3pGSP: 5′-AGCCTGCTGGGGTGGAA-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-181d-5pGSP: 5′-GGGGCATTCATTGTTGTCG-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-23b-3pGSP: 5′-GGGATCACATTGCCAGGG-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-191a-5pGSP: 5′-GGCAACGGAATCCCAAAAG-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-200c-3pGSP: 5′-GGGGTAATACTGCCGGGTAA-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-328a-3pGSP: 5′-AACTCGCCCTCTCTGCCC-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ nutrients-07-01333-t002_Table 2 Table 2 Primers of mRNA targets. [score:1]
Name Primers U6F: 5′-GCTTCGGCAGCACATATACTAAAAT-3′ R: 5′-CGCTTCACGAATTTGCGTGTCAT-3′ rno-miR-500-3pGSP: 5′-GGAAGGCACCTGGGCAAG-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-499-3pGSP: 5′-GGGGAACATCACAGCAAGTC-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-214-3pGSP: 5′-GGGGACAGCAGGCACAGAC-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-20b-5pGSP: 5′-GGGGCAAAGTGCTCATAGTG-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-877GSP: 5′-GGGGAAGTAGAGGAGATGGC-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-451-5pGSP: 5′-GGGGGAAACCGTTACCATTAC-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-3577GSP: 5′-GGGTTCTGTCCCTCTTGGC-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-370-3pGSP: 5′-AGCCTGCTGGGGTGGAA-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-181d-5pGSP: 5′-GGGGCATTCATTGTTGTCG-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-23b-3pGSP: 5′-GGGATCACATTGCCAGGG-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-191a-5pGSP: 5′-GGCAACGGAATCCCAAAAG-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-200c-3pGSP: 5′-GGGGTAATACTGCCGGGTAA-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-328a-3pGSP: 5′-AACTCGCCCTCTCTGCCC-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ nutrients-07-01333-t002_Table 2 Table 2 Primers of mRNA targets. [score:1]
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[+] score: 20
The miR-1 and miR-29a target DnaJ-B1 whereas nucleolin is targeted by miR-23 and miR-1 with a statistical significance (Fig. 12, I&II). [score:5]
MiR-23a seemed to have higher expression in experimental tissues but not statistically significant levels (p = 0.065), whereas miR-23b expression was not altered like in internal control GAPDH (p = 0.13; Fig. 3. II). [score:5]
MiR-29a significantly up-regulates GTA (p<0.01), whereas both miR-1 and miR-23 tend to increase the transport activity (for miR-1 p = 0.06 and 0.08; for miR-23a p = 0.08 and no difference; Fig. 9A, B) compare to the mock treatment. [score:4]
Mimic microRNAs miR-29a and miR-23 up-regulate the glucose transport activities in L6 SKM cell-line as insulin-independent and dependent manner respectively. [score:4]
Precursor microRNA mimics- Mimics of endogenous precursor micro -RNA synthetic molecule for rat, namely, Pre-miR-1, Pre-miR-23a, Pre-miR-23b and Pre-miR-29a were purchased from Ambion Inc. [score:1]
Figure 3 shows the 22 cycles (mid log of exponential phase, data not shown) of end products in RT-PCR reactions for let7a, miR-23a, miR-23b, miR-1 along with GAPDH as an internal control. [score:1]
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[+] score: 18
Of the 46 increased miRNA, sICAM-1 was the predicted target of 6 (miR-23b, miR-27a, miR-99a, miR-100, miR-324-5p, miR-363); PAI-1 was the predicted target of 4 (miR-30a, miR-30d, miR-182, miR-384-5p), E selectin the predicted target of 2 (miR-16; miR-195) and the alpha chain of fibrinogen the predicted target of miR-29c [26]. [score:9]
microRNA-23b regulates the expression of inflammatory factors in vascular endothelial cells during sepsis. [score:4]
Included among the 46 miRNAs with increased expression were 7 (miR-21, miR-16, miR-26a, miR-26b, miR-23a, miR-23b, miR-126) included in surveys of the most abundant miRNAs in human platelets [23, 24] and the miR-126 gene products miR-126-3p and miR-126-5p that are also enriched in vascular endothelial cells and endothelial microparticles [25]. [score:3]
Among the individual miRNAs previously associated with endothelial cell and monocyte activation and sepsis in humans and rodents [27– 29], we found increases in our study of miR-16, miR-21, miR-126, miR-146a, miR-150, miR-511, and miR-23b. [score:1]
Among these, miR-150, miR-23b, and miR-146a have been previously identified as potential circulating mediators or biomarkers of inflammatory pathways in sepsis. [score:1]
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7
[+] score: 17
Other miRNAs from this paper: rno-mir-140, rno-mir-16, rno-mir-203a, rno-mir-203b, rno-mir-15a
MyD88, a key adaptor protein for IL-1R and Toll-like receptors that was recently found to modulate myoblast fusion [33], is targeted by miR-203, and this results in the downregulation of MyD88 expression [34]; miR-15a and miR-16 were shown to repress the expression of Wnt3a [35]; and the miRNA-23b cluster was reported to inhibit the expression of Smad4 [36]. [score:14]
MicroRNA-23b cluster microRNAs regulate transforming growth factor-beta/bone morphogenetic protein signaling and liver stem cell differentiation by targeting Smads. [score:3]
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8
[+] score: 15
Analysis at P21 revealed 74 mature miRNAs with differential expression between LPD -induced IUGR rat lungs and control lungs (Fig 1): 10 showed more than twofold differential expression: miR-184, miR-127-3p, miR-378a-5p and miR541-5p were downregulated, and miR-30e-5p, miR-23b-5p, miR-451-5p, miR-1839-5p, miR-449a-5p, and miR-19b-3p were upregulated in LPD -induced IUGR versus control lungs. [score:11]
Among the other miRNAs found deregulated in our study, miR-34c-5p, miR-128-3p miR-184, miR127-3p, miR-30e-5p, and miR-23b-5p were also previously described as “tumour suppressors”[22– 26], although many miRNA studies previously dealt with cancer or oncogenic proliferation states and the current analysis depended on previous reports. [score:4]
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[+] score: 14
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]
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[+] score: 12
Interestingly, F2-SSS dams showed upregulated miR-23b, which regulates oligodendrocyte development and myelination [49]. [score:6]
The qRT-PCR confirmed changes of the selected miRNAs (Figure  4B), decreased expression of miR-96, miR-141, miR-182, miR-183, miR-200a, miR-200b, miR-429 and miR-451 in F2-SSS compared to F0-S animals, whereas miR-23b and miR-200c showed increased expression levels. [score:4]
In order to validate miRNAs, we performed quantitative real time PCR (qRT-PCR) analysis of these differentially regulated miRNAs (n = 3 per group for F0, F1 and F2 generations, three replicates per sample): miR-23b, miR-96, miR-141, miR-181a, miR-182, miR-183, miR-200a, miR-200b, miR-200c, miR429 and miR-451. [score:2]
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11
[+] score: 12
Other miRNAs from this paper: rno-mir-21, rno-mir-34a
For instance, miR-21 expression was up-regulated during the early phases of LR, which inhibits Peli1 and potentially regulate NF-κB signaling [15]; miR-23b was down-regulated in the termination phase of LR, and may contribute to activation of the TGF-β1/Smad3 signaling [16]. [score:12]
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12
[+] score: 8
Among them, miR-27a-3p, let-7a-5p, miR-10b-5p, and miR-23b-3p have been shown to function as regulators of spinal cord development and remo deling, and have been implicated in diseases of the spinal cord [20, 21]. [score:5]
Nine of the miRs (miR-200b-3p, miR-27a-3p, let-7a-5p, miR-21-5p, miR-10b-5p, miR-23b-3p, miR-221-3p, miR-100-5p, and miR-28-5p) were differently expressed at both 24 and 72 hours after reperfusion. [score:3]
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13
[+] score: 8
By activating TRAF6, synergizing TNF- α expression, and inhibiting miR-23b, NF- κB and other downstream pathways are strongly upregulated [61]. [score:8]
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14
[+] score: 7
We detected a series of miRNAs, but only miR-23a expression was significantly decreased (Figure 2(a)), suggesting that CXCL13 signaling may inhibit miR-23 expression during osteoblast induction. [score:7]
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15
[+] score: 7
Of these, miR-500-3p, miR-23b-3p, miR-200a-3p, miR-19b-3p, miR-92a-1-5p, miR-21-5p, miR-21-3p, miR-1843-3p, miR-223-3p, miR-3473, and miR-129-2-3p were found to be upregulated, whereas miR-92b-3p, miR-3102, and miR-3577 were found to be downregulated in the rat brain. [score:7]
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16
[+] score: 7
Because the target genes of let-7 (MOR) and miR-23b (MOR1) interact with the target gene of miR-365 (β-arrestin 2), we cannot rule out that there may be a relationship between these miRNAs and miR-365. [score:5]
Previous studies have reported that multiple miRNA -based pathways, such as let-7 and miR-23b, contributed to morphine tolerance 10 27, and some of these show the same deregulation pattern of miR-365. [score:2]
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[+] score: 7
Using computer -based predictions miR-23a and miR-23b were identified as the only miRs that target both MAFbx and MuRF1 [4] and reporter gene studies confirmed MAFbx and MuRF1 as targets [36]. [score:5]
As compared to the Sham group, a significant reduction in miR expression was observed in the SCI group for miR-23a, miR-23b, miR-27b and, miR-145 (Fig 2A). [score:2]
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[+] score: 7
Additionally, we examined the effects of other four downregulated miRNAs (miR-23b, miR-92a, miR-27a, and miR-30a; results from microarray). [score:4]
of qRT-PCR validation showed that the expression of miR-23b and miR-145 were indeed reduced by TNF- α in time- and dose -dependent manners (Figures 1f and g). [score:3]
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[+] score: 6
miR-23b acts as a trans-acting factor, which interacts with the k box motif of 3′-UTR of MOR1 to suppress MOR translation efficiency [13]. [score:5]
In addition to let-7 and miR-23b, other miRNAs involved in morphine tolerance include miR-124, miR-190, miR-103 and miR-93-5p [14– 17]. [score:1]
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[+] score: 6
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-24-1, rno-mir-24-2, rno-mir-25, rno-mir-26a, rno-mir-26b, rno-mir-30c-1, rno-mir-30e, rno-mir-30b, 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
Differential expression of miR-23a, miR-23b,miR-542–3p, miR-211, and miR-17–5p in granulosa/cumulus cells from women undergoing assisted reproduction suggests aberrant miRNA expression may be an underlying etiology in female infertility [16, 17]. [score:5]
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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[+] score: 5
Down-regulation of miR-23b contributes to activation of the TGF-b1/Smad3 signalling to terminate liver regeneration 33. miR-376b is involved in the IL6 signaling transduction system to prime liver regeneration 34. miRNAs can regulate lipid and bile acid metabolism which are involved in liver regeneration, thus the miRNAs may affect liver regeneration via lipid and bile acid. [score:5]
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[+] score: 5
Similarly, miR-29a, miR-221 and miR-23b in this network seem to regulate the expression of Vimentin and SLUG indirectly through Caspase 7, AP-1 (activator protein 1) and PAK (p21 protein activated kinase 2). [score:5]
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[+] score: 5
Other miRNAs from this paper: hsa-mir-16-1, hsa-mir-17, hsa-mir-20a, hsa-mir-21, hsa-mir-23a, hsa-mir-100, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-107, hsa-mir-16-2, mmu-mir-1a-1, mmu-mir-23b, mmu-mir-125b-2, mmu-mir-130a, mmu-mir-9-2, mmu-mir-145a, mmu-mir-181a-2, mmu-mir-184, mmu-mir-199a-1, hsa-mir-199a-1, mmu-mir-205, mmu-mir-206, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-199a-2, hsa-mir-205, hsa-mir-181a-1, hsa-mir-214, hsa-mir-219a-1, hsa-mir-223, mmu-mir-302a, hsa-mir-1-2, hsa-mir-23b, hsa-mir-125b-1, hsa-mir-130a, hsa-mir-145, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125b-2, hsa-mir-184, hsa-mir-206, mmu-mir-16-1, mmu-mir-16-2, mmu-mir-20a, mmu-mir-21a, mmu-mir-23a, mmu-mir-103-1, mmu-mir-103-2, rno-mir-338, mmu-mir-338, rno-mir-20a, hsa-mir-1-1, mmu-mir-1a-2, hsa-mir-181b-2, mmu-mir-107, mmu-mir-17, mmu-mir-100, mmu-mir-181a-1, mmu-mir-214, mmu-mir-219a-1, mmu-mir-223, mmu-mir-199a-2, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-181b-1, mmu-mir-125b-1, hsa-mir-302a, hsa-mir-219a-2, mmu-mir-219a-2, hsa-mir-302b, hsa-mir-302c, hsa-mir-302d, hsa-mir-367, hsa-mir-372, hsa-mir-338, mmu-mir-181b-2, rno-mir-9a-1, rno-mir-9a-3, rno-mir-9a-2, rno-mir-16, rno-mir-17-1, rno-mir-21, rno-mir-23a, rno-mir-100, rno-mir-103-2, rno-mir-103-1, rno-mir-107, rno-mir-125b-1, rno-mir-125b-2, rno-mir-130a, rno-mir-145, rno-mir-181a-2, rno-mir-181b-1, rno-mir-181b-2, rno-mir-184, rno-mir-199a, rno-mir-205, rno-mir-206, rno-mir-181a-1, rno-mir-214, rno-mir-219a-1, rno-mir-219a-2, rno-mir-223, hsa-mir-512-1, hsa-mir-512-2, rno-mir-1, mmu-mir-367, mmu-mir-302b, mmu-mir-302c, mmu-mir-302d, rno-mir-17-2, hsa-mir-1183, mmu-mir-1b, hsa-mir-302e, hsa-mir-302f, hsa-mir-103b-1, hsa-mir-103b-2, rno-mir-9b-3, rno-mir-9b-1, rno-mir-9b-2, rno-mir-219b, hsa-mir-23c, hsa-mir-219b, mmu-mir-145b, mmu-mir-21b, mmu-mir-21c, mmu-mir-219b, mmu-mir-219c, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
Another report demonstrates that miR-23 facilitates OL development by negatively regulating lamin B1 (LMNB1), a protein found to repress production of MBP, proteolipid protein 1 (PLP), and myelin oligodendrocyte glycoprotein (MOG) [19]. [score:3]
MiR-23b was also present in high levels during these same stages, although with reduced expression at the OP2 and OP3 stages. [score:2]
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[+] score: 5
In samples of endoscopic pinch biopsies, the expressions of miR-23b, -106, -191, -196, -19b, and -629 have significant changes in colonic mucosa of active Crohn's colitis patients, whereas miR-16, -21, -223, and -594 have been identified to be overexpressed in chronic active ileal CD, which indicates that region-specific IBD -associated miRNAs are involved in diverse pathways responsible for the pathogenesis of different IBD subtypes [1, 43]. [score:5]
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[+] score: 5
After normalizing the signal intensities for all miRNA expression levels, miR-124-3p, miR-9a-3p, miR-34a-5p, miR-9a-5p, miR-125b-5p, miR-let-7c-5p, miR-29a-3p, miR-23b-3p, miR-451-5p, and miR-30c-5p were the miRNAs expressed at the highest levels (Figure  1). [score:5]
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26
[+] score: 5
Other miRNAs from this paper: hsa-mir-17, hsa-mir-18a, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-20a, hsa-mir-21, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-27a, hsa-mir-30a, hsa-mir-32, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-93, hsa-mir-107, hsa-mir-129-1, hsa-mir-30c-2, hsa-mir-139, hsa-mir-181c, hsa-mir-204, hsa-mir-212, hsa-mir-181a-1, hsa-mir-222, hsa-mir-15b, hsa-mir-23b, hsa-mir-132, hsa-mir-138-2, hsa-mir-140, hsa-mir-142, hsa-mir-129-2, hsa-mir-138-1, hsa-mir-146a, hsa-mir-154, hsa-mir-186, rno-mir-324, rno-mir-140, rno-mir-129-2, rno-mir-20a, rno-mir-7a-1, rno-mir-101b, hsa-mir-29c, hsa-mir-296, hsa-mir-30e, hsa-mir-374a, hsa-mir-380, hsa-mir-381, hsa-mir-324, rno-mir-9a-1, rno-mir-9a-3, rno-mir-9a-2, rno-mir-15b, rno-mir-17-1, rno-mir-18a, rno-mir-19b-1, rno-mir-19b-2, rno-mir-19a, rno-mir-21, rno-mir-23a, rno-mir-24-1, rno-mir-24-2, rno-mir-27a, rno-mir-29c-1, rno-mir-30e, rno-mir-30a, rno-mir-30c-2, rno-mir-32, rno-mir-92a-1, rno-mir-92a-2, rno-mir-93, rno-mir-107, rno-mir-129-1, rno-mir-132, rno-mir-138-2, rno-mir-138-1, rno-mir-139, rno-mir-142, rno-mir-146a, rno-mir-154, rno-mir-181c, rno-mir-186, rno-mir-204, rno-mir-212, rno-mir-181a-1, rno-mir-222, rno-mir-296, rno-mir-300, hsa-mir-20b, hsa-mir-431, rno-mir-431, hsa-mir-433, rno-mir-433, hsa-mir-410, hsa-mir-494, hsa-mir-181d, hsa-mir-500a, hsa-mir-505, rno-mir-494, rno-mir-381, rno-mir-409a, rno-mir-374, rno-mir-20b, hsa-mir-551b, hsa-mir-598, hsa-mir-652, hsa-mir-655, rno-mir-505, hsa-mir-300, hsa-mir-874, hsa-mir-374b, rno-mir-466b-1, rno-mir-466b-2, rno-mir-466c, rno-mir-874, rno-mir-17-2, rno-mir-181d, rno-mir-380, rno-mir-410, rno-mir-500, rno-mir-598-1, rno-mir-674, rno-mir-652, rno-mir-551b, hsa-mir-3065, rno-mir-344b-2, rno-mir-3564, rno-mir-3065, rno-mir-1188, rno-mir-3584-1, rno-mir-344b-1, hsa-mir-500b, hsa-mir-374c, rno-mir-29c-2, rno-mir-3584-2, rno-mir-598-2, rno-mir-344b-3, rno-mir-466b-3, rno-mir-466b-4
First, a subgroup of miRNAs (miR-15b-5p, miR-17-5p, miR-18a-5p, miR-19a-3p, miR19b-3p, miR-20a-5p, miR-20b-5p, miR-21-5p, miR-23b-5p, miR-24-3p, miR-27a-3p, miR-92a-3p, miR-93-5p, miR-142-3p, miR-344b-2-3p, miR-431, miR-466b-5p and miR-674-3p) displayed increased expression levels during latency (4 and 8 days after SE), decreased their expression levels at the time of the first spontaneous seizure and returned to control levels in the chronic phase (Fig. 2, Supplementary Fig. S1). [score:5]
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[+] score: 3
MB designed to detect miR-23 served as NC and denatured MB (Den MB) served as a positive control (* p <0.05). [score:1]
miRNA-23 has a completely irrelevant sequence to the let-7b, and thus a MB designed to detect miR-23 served as a NC. [score:1]
Additionally, the negative control group (100 pM MB designed to detect miR-23 was used instead of MB for let-7b) did not produce significant fluorescence with the presence of let-7b mimic, suggesting the MB for let-7b was indeed specific for detecting let-7b. [score:1]
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[+] score: 3
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-mir-18a, hsa-mir-21, hsa-mir-23a, hsa-mir-26a-1, hsa-mir-30a, hsa-mir-99a, hsa-mir-103a-2, hsa-mir-103a-1, mmu-mir-1a-1, mmu-mir-23b, mmu-mir-30a, mmu-mir-99a, mmu-mir-126a, mmu-mir-9-2, mmu-mir-133a-1, mmu-mir-138-2, hsa-mir-192, mmu-mir-204, mmu-mir-122, hsa-mir-204, hsa-mir-1-2, hsa-mir-23b, hsa-mir-122, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-138-2, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-126, hsa-mir-138-1, mmu-mir-192, mmu-let-7a-1, mmu-let-7a-2, mmu-mir-18a, mmu-mir-21a, mmu-mir-23a, mmu-mir-26a-1, mmu-mir-103-1, mmu-mir-103-2, hsa-mir-1-1, mmu-mir-1a-2, mmu-mir-26a-2, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-138-1, hsa-mir-26a-2, hsa-mir-376c, hsa-mir-381, mmu-mir-381, mmu-mir-133a-2, rno-let-7a-1, rno-let-7a-2, rno-mir-9a-1, rno-mir-9a-3, rno-mir-9a-2, rno-mir-18a, rno-mir-21, rno-mir-23a, rno-mir-26a, rno-mir-30a, rno-mir-99a, rno-mir-103-2, rno-mir-103-1, rno-mir-122, rno-mir-126a, rno-mir-133a, rno-mir-138-2, rno-mir-138-1, rno-mir-192, rno-mir-204, mmu-mir-411, hsa-mir-451a, mmu-mir-451a, rno-mir-451, hsa-mir-193b, rno-mir-1, mmu-mir-376c, rno-mir-376c, rno-mir-381, hsa-mir-574, hsa-mir-652, hsa-mir-411, bta-mir-26a-2, bta-mir-103-1, bta-mir-16b, bta-mir-18a, bta-mir-21, bta-mir-99a, bta-mir-126, mmu-mir-652, bta-mir-138-2, bta-mir-192, bta-mir-23a, bta-mir-30a, bta-let-7a-1, bta-mir-122, bta-mir-23b, bta-let-7a-2, bta-let-7a-3, bta-mir-103-2, bta-mir-204, mmu-mir-193b, mmu-mir-574, rno-mir-411, rno-mir-652, mmu-mir-1b, hsa-mir-103b-1, hsa-mir-103b-2, bta-mir-1-2, bta-mir-1-1, bta-mir-133a-2, bta-mir-133a-1, bta-mir-138-1, bta-mir-193b, bta-mir-26a-1, bta-mir-381, bta-mir-411a, bta-mir-451, bta-mir-9-1, bta-mir-9-2, bta-mir-376c, bta-mir-1388, rno-mir-9b-3, rno-mir-9b-1, rno-mir-126b, rno-mir-9b-2, hsa-mir-451b, bta-mir-574, bta-mir-652, mmu-mir-21b, mmu-mir-21c, mmu-mir-451b, bta-mir-411b, bta-mir-411c, mmu-mir-126b, rno-mir-193b, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
In contrast, 15 miRNAs were identified in all tissues and several of them (e. g., miR-23b and -99a) were expressed at high levels in all tissues. [score:3]
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[+] score: 3
2) Some miRNAs, including let-7 family (let-a, -b and -c), miR-16, miR-23b, miR-26, miR-31 and miR-375, were always highly expressed either before or after transdifferentiation (data not shown). [score:3]
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[+] score: 3
We found that miRNAs with higher expression in WBCs includes different miRNA families: mir-15, mir-17, mir-181, mir-23, mir-27 and mir-29 families. [score:3]
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[+] score: 2
Among ncRNAs, some studies have reported that miRNAs are involved in the development of morphine tolerance [7, 8], including the let-7 family, miR-23b [9], miR-133b, miR-339 [10], miR-365 [11] and miR-219-5p [12]. [score:2]
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[+] 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: 1
Normalization was performed to miR-103a-3p, miR-107, miR-181a-3p, miR-181a-5p, miR24-3p, miR-451a, let-7i-5p, and miR23-3p. [score:1]
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[+] score: 1
Circulating exosomal miR-21 has been reported as a biomarker in each tumor stage of colorectal cancer [15] and plasma exosomal miR-23b-3p, miR-10b-5p and miR-21-5p have been reported as prognostic biomarkers for non-small-cell lung cancer [16]. [score:1]
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[+] score: 1
In spinal cord injury, inthathecal injections of miR-23b attenuate mechanical and thermal pain (Im et al., 2012). [score:1]
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[+] score: 1
MicroRNA profiling identified several miRNAs that have been previously associated with cardiac hypertrophy such as miR-214, miR-23b, miR-15b, rno-miR-26b, rno-miR-221, rno-miR-222, rno-miR-107 [59], miR-23a, miR-208, rno-miR-133b, miR-19a and mi-r133a [60]. [score:1]
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[+] score: 1
These include miR-103 [18], miR-124 [20], miR-23b [21] and miR-7a [22]. [score:1]
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[+] score: 1
Effect of miR-23 on oxidant -induced injury in human retinal pigment epithelial cells. [score:1]
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[+] score: 1
Stress also led to critical decreases in let-7c, miR-23b, miR-181, and miR186 amounts. [score:1]
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