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35 publications mentioning rno-mir-98

Open access articles that are associated with the species Rattus norvegicus and mention the gene name mir-98. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

[+] score: 298
Figure 4MiR-98 overexpression inhibits the expression of Fas and caspase-3. (A) and (B) MiR-98 overexpression significantly prevented upregulation of Fas mRNA and protein level in H [2]O [2] -treated NRVCs. [score:11]
MiR-98 overexpression suppresses H [2]O [2] -induced upregulation of Fas and caspase-3 in cardiomyocytesWe next aimed to explore the underlying mechanism that miR-98 inhibited H [2]O [2] -induced apoptosis. [score:10]
n = 6. (B) Bcl-2 expression was suppressed by H [2]O [2] but upregulated by miR-98. [score:8]
MiR-98 overexpression suppresses H [2]O [2] -induced upregulation of Fas and caspase-3 in cardiomyocytes. [score:7]
As shown in Fig.   4A, compared with control group, Fas mRNA expression was significantly upregulated in the H [2]O [2] -treated NRVCs, which could be reversed by miR-98 overexpression. [score:7]
As Fas and caspase-3 were proved to be the target genes of miR-98 17, 18, we further verified the expression of Fas and caspase-3 in the presence of miR-98 overexpression. [score:7]
MiR-98 overexpression led to the decreased Fas protein expression in posttranscriptional level (Fig.   4B), further indicating that Fas was the target gene of miR-98. [score:7]
miR-98 overexpression significantly inhibited luciferase activity in the wild-type group, demonstrating that miR-98 could target at 3′-UTR of Fas (Fig.   5B). [score:7]
Meanwhile, miR-98 overexpression also reduced the upregulation of caspase-3 mRNA induced by H [2]O [2] (Fig.   4C). [score:6]
NRVCs were transfected with NC (negative control), miR-98 mimic (miR-98 mim), miR-98 inhibitor (miR-98 inh), and miR-98 mimic + inhibitor (miR-98 mim&inh) and then treated with H [2]O [2] (100 μM) for 4 h. (A) MTT assay suggested that miR-98 mimic restored cell viability of NRVCs treated with 100 μM H [2]O [2] for 4 h. n = 8. (B) Statistical results of TUNEL -positive cells per field indicated that miR-98 mimic suppressed H [2]O [2] treatment -induced cell apoptosis. [score:6]
In addition, miR-98 was verified to target Fas directly and regulated Fas -mediated apoptosis in HeLa cells [18]. [score:5]
Yang Y Ago T Zhai P Ab dellatif M Sadoshima J Thioredoxin 1 negatively regulates angiotensin II -induced cardiac hypertrophy through upregulation of miR-98/let-7Circ Res. [score:5]
n = 5. (C) and (D) The mRNA and protein expression of caspase-3 were also remarkably elevated by H [2]O [2] but reduced by miR-98 overexpression. [score:5]
The current results showed that overexpression of miR-98 reversed the reduction in Bcl-2 expression caused by acute ischemia, suggesting that Bcl-2 is involved in miR-98 -induced cardioprotection. [score:5]
Also, Bcl-2 expression was elevated in NRVCs after miR-98 overexpression (Fig.   3B). [score:5]
Fas and caspase-3 expression were also involved in this research because they were the key modulators of apoptosis and can be regulated by miR-98 17, 18. [score:4]
Yuan Y MicroRNA-98 and microRNA-214 post-transcriptionally regulate enhancer of zeste homolog 2 and inhibit migration and invasion in human esophageal squamous cell carcinomaMol Cancer. [score:4]
However, miR-98 overexpression induced a sharp decrease of Bax expression in NRVCs compared with NC group (Fig.   3A). [score:4]
Our work demonstrated that miR-98 was upregulated in MI mice and in oxidative stress-stimulated cardiomyocytes. [score:4]
However, the mechanism by which miR-98 reduced the apoptosis of cardiomyocytes through targeting Fas/Caspase-3 and simultaneously regulating mitochondrial apoptotic pathway remains to be elucidated. [score:4]
In addition, miR-98 targeted at the ACUACCUC sequence in the 3′-UTR of Fas mRNA directly to reduce Fas protein production. [score:4]
Overexpression of miR-98 attenuated the deterioration of left ventricular performance, as indicated by the increased EF and FS (Fig.   7C–E). [score:3]
n = 3. (C) miR-98 expression level in NRVCs after miR-98 mimic transfection. [score:3]
Recently, altered miR-98 expression has been found in several carcinomas [14]. [score:3]
Figure 2Overexpression of miR-98 prevents cardiomyocyte apoptosis in response to H [2]O [2]. [score:3]
n = 5. (E) MiR-98 significantly prevented upregulation of Fas mRNA level in the infarcted and border zones of MI mice. [score:3]
Real-time PCR analysis revealed that the expression of miR-98 in the infarcted and border zones of rat hearts at 3 days after MI was much lower than that in sham-operated animals (Fig.   1B). [score:3]
Meanwhile, we also examined the expression of miR-98 in heart tissues after MI for 3 days. [score:3]
Figure 3Effect of miR-98 on Bax and Bcl-2 expression and mitochondrial membrane potential (Δψm). [score:3]
As shown in Fig.   1D, 1, 2 and 3 days after injection of miR-98 agomir using our delivery method, miR-98 expression was markedly increased in the heart tissue. [score:3]
Real-time PCR analysis revealed that Fas mRNA levels were markedly increased in infarcted and border zones and the existence of miR-98 agomir led to the decreased expression of Fas in transcriptional level (Fig.   6E). [score:3]
At the same time, miR-98 significantly reversed the expression of Fas protein. [score:3]
However, H [2]O [2] -induced increase in monomeric form cells was reduced by miR-98 overexpression (Fig.   3C and D). [score:3]
Taken together, these results proved that miR-98 overexpression prevented H [2]O [2] -induced cardiomyocyte apoptosis and promoted cell survival. [score:3]
Western blot showed that the expression caspase-3 was significantly decreased by miR-98. [score:3]
Then, we overexpressed miR-98 in NRVCs by miR-98 mimic transfection and in mice hearts by miR-98 agomir injection. [score:3]
Figure 5Fas was the target gene of miR-98. [score:3]
Therefore, Fas was proved to be the target gene of miR-98. [score:3]
Cardiomyocytes were starved in serum-free medium for 24 hours, and then transiently transfected with miR-98 mimic (50 nM), miR-98 inhibitor (100 nM) and NC (50 nM), using X-treme GENE siRNA transfection reagent (Roche, Penzberg Germany) according to the manufacturer’s instructions. [score:3]
Overexpression of miR-98 decreases infarct size and improves cardiac function of infarcted heart in mice. [score:3]
Our findings suggest that miR-98 may provide a potential novel therapeutic approach for the treatment of ischemic heart disease. [score:3]
MiR-98 is downregulated in response to myocardial ischemic injury. [score:3]
Overexpression of miR-98 attenuated apoptosis in H [2]O [2] -treated NRVCs and MI mice mo del. [score:3]
MiR-98 overexpression prevented H [2]O [2] -induced cardiomyocyte apoptosisBased on the above results, we subsequently aimed to evaluate the effects of miR-98 overexpression on cell apoptosis. [score:3]
Moreover, overexpression of miR-98 also increased cell viability and prevented cell necrosis in H [2]O [2] -treated NRVCs (Fig.   2F and G). [score:3]
This reveals that overexpression of miR-98 during the infarct period might be a useful approach for heart protection. [score:3]
We next aimed to explore the underlying mechanism that miR-98 inhibited H [2]O [2] -induced apoptosis. [score:3]
Due to the non-homology of Fas in different species, we used computational methods to search for the potential targets of miR-98 in rats and constructed luciferase reporter plasmids containing the 3′-UTR of Fas. [score:3]
Firstly, the expression of miR-98 was detected in H [2]O [2] -treated cardiomyocytes and postinfarct cardiac tissues. [score:3]
In total, the present study demonstrates that miR-98 suppresses the apoptosis of cardiomyocytes, reduces the MI size, and improves the cardiac function. [score:3]
n = 6. (D) miR-98 expression level in rat ventricles after administration with miR-98 agomir. [score:3]
By contrast, the number of JC-1 monomeric cells was markedly reduced in NRVCs overexpressed miR-98. [score:3]
Li H miR-98 protects endothelial cells against hypoxia/reoxygenation induced-apoptosis by targeting caspase-3Biochem Biophys Res Commun. [score:3]
Furthermore, the effect of miR-98 mimic on H [2]O [2] -induced cell apoptosis was abolished by co-transfection with miR-98 inhibitor (Fig.   2D and E). [score:3]
Effect of miR-98 overexpression on ischemia -induced cardiomyocyte apoptosis. [score:3]
MiR-98 overexpression regulates apoptosis-related proteins and mitochondrial membrane potential. [score:3]
Furthermore, it was observed that the number of TUNEL -positive cells was significantly increased in H [2]O [2] group, which was diminished by miR-98 mimic but not by NC or miR-98 inhibitor (Fig.   2B and C). [score:3]
Moreover, miR-98 has been reported to be a sensitive marker of renal ischemic injury [16] and protect endothelial cells against hypoxia/reoxygenation induced-apoptosis by targeting caspase-3 [17]. [score:3]
MiR-98 -mimic, miR-98 inhibitor and NC were synthesized by Guangzhou RiboBio (Guangzhou, China). [score:3]
MiR-98 directly targets at the 3′-UTR of Fas. [score:3]
Fas and caspase-3 were identified to be the target genes of miR-98 in humans 17, 18 and the predicted site in caspase-3 3′-UTR showed a good conservative character among different species [17]. [score:3]
The cardioprotective effect of miR-98 was achieved by regulating Fas/Caspase-3 apoptotic signal pathway. [score:2]
MiR-98 overexpression markedly decreased the relative luciferase activity in the WT 3′-UTR but not mutant 3′-UTR of Fas mRNA. [score:2]
In contrast, compared with miRNA negative control (NC) transfection group, miR-98 overexpression by transfecting with miR-98 mimic significantly increased the cell viability of NRVCs treated with H [2]O [2] (Fig.   2A). [score:2]
As shown in Fig.   1A, compared with control group, miR-98 expression was significantly decreased by exposure to 100 μM H [2]O [2] in NRVCs. [score:2]
In this study, we found that Fas and caspase-3 were negatively regulated by miR-98. [score:2]
MiR-98 overexpression prevented H [2]O [2] -induced cardiomyocyte apoptosis. [score:2]
Consequently, we acknowledged from this study that miR-98 could negatively regulate MI injury -induced cell apoptosis possibly through Fas and caspase-3 pathway. [score:2]
Since miR-98 promoted cell survival and prevented cardiomyocyte apoptosis, we further investigated its role in regulating the expression of apoptosis-related proteins and mitochondrial membrane potential (Δψm ). [score:2]
n = 5. (F) MiR-98 suppressed the elevation of caspase-3 mRNA level in the infarcted, border and remote zones of MI mice. [score:2]
Wang S Let-7/miR-98 regulate Fas and Fas -mediated apoptosisGenes Immun. [score:2]
MiR-98 is one of the members of the let-7 miRNA family, which is first discovered to control the developmental timing of cell differentiation and proliferation in C. elegans 12, 13. [score:2]
Figure 7Reduction of infarct size and improvement of cardiac function by miR-98 in MI mice. [score:1]
We then tried to clarify whether antiapoptotic effects of miR-98 on cultured cells under H [2]O [2] conditions also exist under in vivo conditions in MI. [score:1]
Moreover, the activity of serum lactate dehydrogenase (LDH) (a marker for cardiac injury) increased obviously after MI, which was significantly attenuated by miR-98 agomir as well (Fig.   6C). [score:1]
The ascending aortic artery and the main pulmonary artery were clamped; then, miR-98 agomir (200 nmol·kg [−1] at the volume of 80 μL) was injected into the left ventricular cavity through the tip of the heart with a 30-gauge syringe. [score:1]
The levels of miR-98, caspase-3 and Fas mRNA were determined using SYBR Green incorporation on Roche Light-Cycler 480 Real Time PCR system (Roche, Germany), with U6 as an internal control for miR-98 and GAPDH for caspase-3 and Fas. [score:1]
Therefore, we have demonstrated for the first time that miR-98 protects against H [2]O [2] -induced mitochondrial dysfunction in NRVCs. [score:1]
The protein level of caspase-3 after miR-98 mimic transfection showed the similar trend with the mRNA level (Fig.   4D). [score:1]
Therefore, let-7/miR-98 miRNAs are considered as an oncomir family crucial in regulating cell cycle and apoptosis [15]. [score:1]
As expected, this elevation of caspase-3 activity was blocked by miR-98 agomir administration. [score:1]
Firstly, to investigate the effects of miR-98 on mitochondrial protection, we analyzed the expression of Bcl-2 and Bax and the mitochondrial membrane potential (Δψm). [score:1]
Consequently, miR-98 could reverse the H [2]O [2] induced elevation of Fas and caspase-3, and thus provide protections against ischemia -induced cardiomyocyte apoptosis. [score:1]
We found that the apoptosis percentage was increased by H [2]O [2] treatment, which was significantly diminished by miR-98 mimic (Figure 2 D and E). [score:1]
n = 6. (C) Serum lactate dehydrogenase (LDH) activity is increased in MI mice and restored by miR-98 agomir administration. [score:1]
However, miR-98 failed to affect the luciferase activity elicited by the construct carrying the Fas 3′-UTR with the mutant miR-98 -binding site (Fig.   5C). [score:1]
MI Mo del and Administration of miR-98 agomir. [score:1]
To determine the change of miR-98 in the different areas of infarcted hearts, miRNAs were isolated from infarcted zone, border zone and remote zone. [score:1]
The miR-98 agomirs (Ribo-bio, Guangzhou, China) are double-stranded RNA analogues identical to the mature mmu-miR-98–5p (5′-UGAGGUAGUAAGUUGUAUUGUU-3′). [score:1]
Meanwhile, miR-98 reduced the activation of Bax. [score:1]
Therefore, we speculated that miR-98 simultaneously modulated of the intrinsic and extrinsic pathways of myocardial apoptosis in MI. [score:1]
We then transfected HEK293T cells with the luciferase vector containing a wild-type or mutant miR-98 response element. [score:1]
The binding sites of miR-98 in the 3′-UTR of wild-type Fas mRNA were displayed, but mutant mRNA had few binding sites (Fig.   5A). [score:1]
n = 6. (D) Caspase-3 activity is promoted in MI mice and reversed by miR-98 agomir. [score:1]
In addition, flow cytometry was utilized to validate the protective role of miR-98 in H [2]O [2] -induced cardiomyocyte apoptosis. [score:1]
Then, HEK293T cells were seeded in a 96-well plate and co -transfected with 0.5 μg plasmid and miR-98 mimics or negative controls using Lipofectamine 2000 reagent. [score:1]
Meanwhile, caspase-3 mRNA levels were significantly increased in the whole heart, which could be prevented by miR-98 agomir (Fig.   6F). [score:1]
We detected the functional role of miR-98 agomir in infarcted heart and found that miR-98 agomir significantly reduced the infarct size in MI (Fig.   7A and B). [score:1]
Based on the above results, we subsequently aimed to evaluate the effects of miR-98 overexpression on cell apoptosis. [score:1]
Before coronary artery ligation, miR-98 agomir was administered, which caused a continuous elevation of miR-98 (Fig.   1D). [score:1]
n = 6. (C) Upper panels show representative fluorescent images of JC-1 monomeric mitochondria showing green fluorescence and JC-1 aggregated mitochondria from Control, H [2]O [2], H [2]O [2] + NC and H [2]O [2] + miR-98 mimic groups. [score:1]
We validated the miR-98 level using Real-time PCR, and found that miR-98 level was significantly higher in miR-98 mimic transfection group than that in non-transfection group (Fig.   1C). [score:1]
However, the role of miR-98 in MI -induced cardiomyocyte apoptosis remains unknown. [score:1]
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[+] score: 173
In summary, severe burn injury -induced internal organic hyperpermeability was mediated by upregulated miR-98 expression that inhibited FIH-1 protein expression to the extent that it activated HIF-1 gene expression, resulting in junction -associated protein deficiency. [score:12]
Thus, our results provided the possible therapeutic target that elevated FIH-1 by inhibiting miR-98 results in accumulation of HIF-1 -mediated adaptive cellular responses to burn -induced ischemia and upregulation of the expression of junction -associated genes that protects against burn -induced internal organ epithelial barrier dysfunction. [score:10]
When miR-98 was overexpressed by miR-98 mimic transfection, FIH 3'UTR activity was decreased (Figure  3D) and FIH-1 protein level was downregulated, while HIF-1 protein was upregulated (Figure  3E). [score:9]
Knock down of miR-98 by miR -inhibitor (A) increased FIH 3ʹUTR activity, (B) suppressed HIF-1 expression, and (C) inactivated HIF-1 transcription. [score:8]
So, targeting miR-98 that mediate FIH-1 gene expression suppression demonstrates a therapeutic potential to improve vascular barrier function during burn injury. [score:7]
Protein levels are represented by Western blot in Figure  4A and the result showed a reversing effect of silenced miR-98 on burn serum-reduced FIH-1 expression and burn serum -induced FIH-1 expression as well as burn serum-reduced ZO-1 expression. [score:7]
Overexpression of miR-98 by miR-98 mimic transfection (D) inhibited FIH 3ʹUTR activity, (E) promoted HIF-1 expression, and (F) increased HIF-1 transcription activity. [score:7]
From the result, we found out that miR-98 are the key regulators in burn -induced internal organ endothelial dysfunction via inhibiting FIH-1 expression. [score:6]
In vitro, burn serum stimulation increased rat aorta endothelial monolayer cell permeability as well as upregulated miR-98 expression (P < 0.05). [score:6]
As shown in Figure  5A, co -transfected miR-98 inhibitor with siRNA-FIH-1 reversed silenced miR-98-reduced ZO-1 expression. [score:5]
Importantly, we identify the possible target FIH-1 by miR-98 by result of fluorescent report assay which was further confirmed by protein expression assay showing that silenced miR-98 promoted FIH-1 expression followed with a decreased HIF-1 protein level. [score:5]
To investigate the regulating role of miR-98 in FHI-1 expression in rat aorta endothelial cell, miR-98 was knocked down by cells transfected with miR-98 inhibitor. [score:5]
Figure 3Regulated role of miR-98 in FIH-1 expression in rat aorta endothelial cell. [score:4]
miR-98 negatively regulated FIH-1 expression in rat aorta endothelial cell. [score:4]
Interestingly, we found upregulated miR-98 in rat mo dels of burn and burn serum-stimulated rat vascular endothelial cells. [score:4]
In other experiments, using the same culture conditions to establish TEER ≥ 20 ohm × cm [2], RAECs were transfected with miR-98 inhibitor and/or control siRNA or sequence specific siRNA directed against FIH-1 in 10% fetal bovine serum (FBS) for 24 h. The lung tissues were homogenized and analyzed for HIF-1α, FIH-1, and junction -associated proteins by Western blotting. [score:4]
Incubation cells with burn serum led to miR-98 upregulation (Figure  2A) that corresponds to the observation in Figure  1B. [score:4]
As shown in the result of transfection experiment, miR-98 negatively regulated FIH-1 and tight junction -associated protein expression (P < 0.05). [score:4]
In view of the above result, expression change of miR-98 would influence burn -induced vascular hyperpermeability. [score:3]
Our data support that major burn injury induces miR-98 accumulation, which suppressed FIH-1 gene transcription, leading to loss of tight junction -associated ZO-1 protein and the subsequent increase in lung microvascular barrier permeability. [score:3]
In view of our previous observations that miR-98 inhibitor treatment can increase FIH-1 expression and reversed burn -induced permeability, we next investigated the outcome of siRNA -mediated gene depletion of HIF-1 on the silenced miR-98-reduced monolayer endothelial cell permeability. [score:3]
Cells were pretreated with siRNA-FIH-1 followed by transfection with miR-98 inhibitor. [score:3]
Among these, miR-98 was found expressed to the greatest extent during hypoxia in squamous cell carcinoma [14]. [score:3]
After transfected with miR-98 inhibitor for 48 h, cells were incubated with burn serum or normal serum (as control) followed. [score:3]
For miR-98 expression analysis, total RNAs were extracted with Trizol reagent (Invitrogen, Carlsbad, CA, USA) according to the protocols of the manufacturer followed by DNA-free DNase treatment (Ambion, Austin, TX, USA). [score:3]
Rat aorta endothelial cells were pretreated with miR-98 inhibitor and then stimulated with burn serum. [score:3]
The results showed that the abrogating effect of silenced miR-98 on burn serum-reduced transendothelial electrical resistance was inhibited by siRNA-FIH-1 treatment (Figure  5B). [score:3]
MiR-98 predication of potential targets FIH-1 3'UTR was performed with miRanda software. [score:3]
Rat aortic endothelial cells (2 × 10 [5]) were transfected with 10 to 50 nM anti-miR-98 miRNA inhibitors (Ambion, Austin, TX, USA) or scrambled control (Negative Control 1; Ambion) by using Lipofectamine 2000 from Invitrogen (Carlsbad, CA, USA) according to the manufacturer’s protocol. [score:3]
The findings of the present study suggest severe microvascular permeability due to burns; and the underlying mechanism bases on the promotion of miR-98 level to the extent that it activated HIF-1 gene expression, resulting in junction -associated protein deficiency. [score:3]
Rat aorta endothelial cells were incubated with burn serum for 12 h. (A) Level of miR-98 expression was determined using quantitative real-time PCR. [score:3]
Level of miR-98 and protein of hypoxia-inducible factor-1 (HIF-1), factor inhibiting HIF-1α (FIH-1), and tight junction -associated proteins were determined. [score:3]
And abrogating effect of silenced miR-98 on burn serum-increased albumin permeability was also suppressed (Figure  5C). [score:3]
Especially, miR-98, a subset of HIF-1-inducible miRNAs, was found expressed to the greatest extent during ischemia [19]. [score:3]
Knock down FIH-1 abrogated silenced miR-98-reduced permeability in rat aorta endothelial cells. [score:2]
Figure 4Silenced miR-98 abrogated burn serum-increased permeability in rat aorta endothelial cells. [score:1]
Figure 5Co-silenced FIH-1 abrogated silenced miR-98-reduced permeability in rat aorta endothelial cells. [score:1]
Figure 6 Signaling mechanism by which miR-98 mediated burn -induced increase of microvascular permeability. [score:1]
We hypothesized the possible involvement of miR-98 in acute post-burn pathophysiologic process. [score:1]
This was supported by monolayer endothelial cell analysis showing that silenced miR-98 reversed burn serum -induced junction -associated ZO-1 protein as well as hyperpermeability. [score:1]
These data strongly verify our hypothesis on the possible involvement of miR-98 in acute post-burn pathophysiologic process. [score:1]
Silenced miR-98 abrogated burn serum-increased permeability in rat aorta endothelial cells. [score:1]
Burn FIH-1 miR-98 HIF-1α Microvascular permeability The skin serves as a vital protective barrier against exterior harmful factors, and the disruption of its integrity can lead to patients’ significant disability or even death. [score:1]
Organic microvascular permeability began to rise at 2 h post-burn and maintained the same character throughout the experiment except in lung tissue that was still rising at 12 h; the serum level of miR-98 was elevated (P < 0.05). [score:1]
The plasma was aliquoted and stored at −80°C for miR-98 detection. [score:1]
Fragments of 3'UTR of FIH-1 gene harboring the predicted miR-98 -binding sites were cloned into the firefly luciferase reporter plasmid pMIR-Report (Ambion) according to the manufacturer’s protocol. [score:1]
The results also showed the abrogating effect of silenced miR-98 on burn serum-reduced transendothelial electrical resistance and increased albumin permeability suggesting a protective effect of silenced miR-98 on endothelial cell monolayer permeability. [score:1]
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[+] score: 56
For instance, miR-98 could target IL10, which then up-regulate TNF, which induces the expression of the transcription factor HSF1 (Figure 6), to carry out immune functions. [score:8]
RDX could first up-regulate the expression of miR-71, miR-27ab, miR-98, and miR-135a, then reduce the expression of the gens POLE4, C5ORF13, SULF1 and ROCK2, and eventually induce neurotoxicity. [score:8]
MiRNAs Target Genes Names Regulation Up Down miR-135a Up KIAA1033, CEP350, ROCK2 miR-320 Down BANP, CALD1, POLE4 miR-98 Up SULF1 miR-129* Down BANP, FAM82A2 miR-27ab Up HMGCR, LITAF, NPTX2 CALD1, C5orf13, KIAA1033 miR-342-3P Down VGF KIAA1033 miR-7a Up SLC38A2 POLE4, SLC35E4, C5orf13 miR-674-5p Up VGF Biological functional analysis revealed that more than half (8) of the overlapped genes are involved in neurological diseases and nervous system function (Table 4). [score:6]
MiRNAs Target Genes Names Regulation Up Down miR-135a Up KIAA1033, CEP350, ROCK2 miR-320 Down BANP, CALD1, POLE4 miR-98 Up SULF1 miR-129* Down BANP, FAM82A2 miR-27ab Up HMGCR, LITAF, NPTX2 CALD1, C5orf13, KIAA1033 miR-342-3P Down VGF KIAA1033 miR-7a Up SLC38A2 POLE4, SLC35E4, C5orf13 miR-674-5p Up VGFBiological functional analysis revealed that more than half (8) of the overlapped genes are involved in neurological diseases and nervous system function (Table 4). [score:6]
RDX could first induce the expression of miR-71, miR-27ab, miR-98, and miR-135a, then reduce the expression of POLE4, C5ORF13, SULF1 and ROCK2, and finally induce neurotoxicity. [score:5]
The induction of miR-71, miR-27ab, miR-98, and miR-135a expression by RDX, could reduce the expression of the genes POLE4, C5ORF13, SULF1 and ROCK2, and eventually induce neurotoxicity. [score:5]
As shown in table 3 the targets of miR-135a, miR-98, and most of the targets of miR-7a have an inverse relationship with their responsive miRNAs. [score:5]
RDX could first induce the expression of miR-71, miR-27ab, miR-98, and miR-135a, then reduce the expression of POLE4, C5ORF13, SULF1 and ROCK2, and finally induce neurotoxicity, which provides an alternative mechanism to explain RDX induced neurotoxicity. [score:5]
Of these 9 miRNAs, 6 miRNAs including miR-98, miR-27b, miR135a, miR-7a, miR-674-5p and miR-27a were significantly up-regulated by RDX. [score:4]
Two miRNAs miR-98 and miR-7a were induced in rat brain tissues after exposure to RDX, and they were also up-regulated in mouse brain tissues treated with RDX [11]. [score:4]
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[+] score: 48
Other miRNAs from this paper: hsa-mir-16-1, hsa-mir-98, hsa-mir-16-2, rno-mir-16
However, inhibition of miR-98-3p did up-regulate HDAC activity and greatly inhibited HAT activity. [score:8]
Mimics and inhibitors for miR-98-3p, positive controls, including a miRNA mimic that inhibits GAPDH and a miRNA mimic that increases miR-16, and two negative controls (mimic and inhibitor) were used to assess the transfection efficiency and viability by comparing with a transfection reagent-only control and an untreated control. [score:7]
As mir-98 down-regulation in the cerebellum has been associated with AD and with neuroprotection [37, 38], we examined whether this miRNA could regulate the neuroprotective profile observed. [score:5]
Fig. 3Each diet group and age elicits its own miRNA expression profile but miR-98-3p is overexpressed in all CR and LA diets and may affect HAT and HDAC activity. [score:5]
However, a single miRNA (miR-98-3p) was significantly overexpressed in all groups of CR rats and/or rats fed LA-supplemented diets (Fig.   3b). [score:3]
b qPCR confirmation of RNA-seq results, showing miR98-3p differential expression in all CR and LA supplemented diets. [score:3]
One miRNA, miR-98-3p, showed consistent overexpression in CR and LA supplementation of the diet in our study. [score:3]
We find a single microRNA, miR-98-3p, that is overexpressed during CR feeding and LA dietary supplementation; this microRNA alters HDAC and histone acetyltransferase (HAT) activity, which suggests a role for HAT/HDAC homeostasis in neuroprotection. [score:3]
Increasing miR-98-3p (using a mimic) did not alter HDAC or HAT activity, suggesting that LA -induced inhibition of HDAC activity is not elicited through mir-98-3p. [score:3]
These results suggest that miR-98-3p is a candidate regulator of the neuroprotective profile by maintaining the HAT/HDAC balance and hence acetylation equilibrium. [score:2]
The figure shows that the miR-98-3p inhibitor significantly (p < 0.001, two-tailed t-test) decreases HAT activity when compared with HDAC activity. [score:2]
Using CTX TNA2 cells (rat astrocytes derived from the cerebral cortex), we transfected miR-98-3p inhibitors and mimics, and measured HDAC and HAT activity (Fig.   3c). [score:1]
We also propose that this neuroprotective effect of CR and LA is driven by changes in histone deacetylase (HDAC) and histone acetyltransferase (HAT) homeostasis and implicate a miRNA (miR-98-3p) in this process. [score:1]
mir-98-3p is highlighted by a green box. [score:1]
A miR-98-3p mimic appears not to affect HDAC/HAT balance (no statistically significant difference). [score:1]
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[+] score: 29
In the telencephalon, expression levels of miR-98 increased over four-fold between E12 and E19, a similar finding to that of Sempere and colleagues [15], who found mir-98 expression levels progressively accumulated upon neuronal differentiation in both mouse and human embryonic carcinoma cells. [score:5]
Prominent among this group were miRNAs that are enriched in neurons and associated with developmental regulation (let-7i, let-7f, let-7b, miR-98), cell cycle regulation (miR-137, mIR-128) and neural activity (miR-132, miR-212). [score:4]
In support of a role for miR-98 in telencephalon development, mir-98 overexpression was found to significantly decrease the activity of a luciferase reporter gene fused to the cytoplasmic linker associated protein 2 (Clasp2) 3’-UTR. [score:4]
Enriched ontologies of putative target genes of miR-98, miR-212 and miR-137 were identified using the DAVID online database. [score:3]
To generate reporter vectors bearing binding sites for the three miRNA examined in detail, miR-98, miR-212 and miR-137, oligonucleotides encoding target gene miRNA recognition elements (MREs) were annealed to form SpeI and HindIII restricted overhangs of a ligatable cassette compatible with SpeI and HindIII digested pMIR-REPORT vector (Ambion, Austin, TX) as described previously [69, 70]. [score:3]
In particular, regulation of 3’-UTR elements from Wnt7a (miR-137) and Gpr88 (miR-137) was particularly strong and, along with Clasp2 (miR-98) and Rab15 (miR-212) provides support for the role of post-transcriptional regulation in axon and dendritic growth, maturation and function [35– 38]. [score:3]
Microarray expression data was validated by RT-PCR for miR-98 (B), miR-212 (E) and miR-137 (H) with correlation coefficients of 0.64 (C), 0.62 (F) and 0.69 (I) respectively. [score:3]
Figures show the normalised signal intensity values for miR-98 (A) and miR-212 (D) and miR-137 (G) at each developmental stage in the mesencephalon and telencephalon (*** = p < 0.001). [score:2]
Mir-98 is a member of the let-7 family, highly conserved across species in sequence and function and involved in the developmental timing of cell fates (reviewed [40]). [score:2]
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[+] score: 25
For that reason, rather than selecting the common targets to both algorithms, we chose PicTar algorithm to match upregulated miRNAs (miR-21, miR-98, miR-27a, miR-143, let-7d, miR-126, miR-22) with downregulated putative targets in Ortis et al. and vice versa (Table 4). [score:11]
Using quantitative PCR -based high throughput analysis, we have confirmed upregulation of 7 (miR-21, miR-98, miR-27a, miR-143, let-7d, miR-126, and miR-22) and downregulation of 1 (miR-129) miRNAs out of the 26 activated miRNAs identified in our settings. [score:7]
Eight miRNAs from the PCR-confirmed 11 miRNAs, are common to both in vitro and in vivo inflammation conditions; 7 upregulated (miR-21, miR-98, miR-27a, miR-143, let-7d, miR-126 and miR-22) and one (miR-129) downregulated (Table 3). [score:7]
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[+] score: 19
As a static score of 0.63 indicated its enhanced regulation on the cardiac-specific PPI network, abnormal expression of miR-98 in MI might strongly imbalance its controlled biological modules. [score:4]
The result demonstrated that miR-1 stressed upon regulation of myocyte growth, yet miR-29b and miR-98 put their regulatory emphases upon fibrosis and inflammation, respectively. [score:3]
The modules regulated by miR-1, miR-29b and miR-98 contained more proteins encoded by ischemia related genes (Figure 3). [score:2]
They were miR-1 emphasizing on cell growth regulation, miR-29b stressing on fibrosis and miR-98 focusing on inflammation. [score:2]
Among the 18 PRmiRs, miR-98 showed the most efficient gene regulation (dynamic score: 0.778, Figure 2C). [score:2]
Further finding revealed that miR-1 focused on regulation of myocyte growth, yet miR-29b and miR-98 stressed on fibrosis and inflammation, respectively. [score:2]
A-C. Largest functional modules regulated by miR-1, miR-29b and miR-98, respectively. [score:2]
Our network analysis identified that, among these miRNAs, the prime players in MI were miR-1, miR-29b and miR-98. [score:1]
Although the important role of miR-98 in inflammatory response of cholangiocyte has been verified [32], the experimental evidence of its involvement in inflammation during myocardial ischemia still lacks. [score:1]
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[+] score: 18
This would likely be the case for the observed increases in the expression of the cell death inducers caspase 3 [69], [70] and Fas [71], the expression of which parallels the decreased expression of their regulators, the let7/miR-98 family members miR-96 and miR-146a. [score:8]
Moreover, the microRNAs miR-103, miR-107, miR-133a, miR-145, mir146a and miR-98, which presented altered expression at 7 days after SCI in both Liu's study [6] and ours, demonstrated significant alterations in the expression of their targets, according to De Biase et al. [7]. [score:7]
The effect of changes in the expression of other microRNAs, such as members of the let7/miR-98 family, remains controversial because they display variable roles in apoptosis depending on the circumstances (see Table 7). [score:3]
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[+] score: 17
Four differentially expressed miRNAs in the lung had functions in cell differentiation, protein expression and apoptosis, including promotion of muscle differentiation (miR-206), regulation of cholangiocyte expression factor (miR-98), targeting pro-apoptotic and antiapoptotic proteins (miR-494), myeloid lineage development and promoting granulocytic differentiation, and suppression of erythrocytic differentiation (miR-223). [score:13]
Various other miRNAs, such as miR-29c and miR-98, were differentially expressed in the spleen and lungs of the infected animals respectively. [score:3]
It was found that miR-494, miR-365 and miR-451 were present in liver, miR-206, miR-468 and miR-691 in spleen, and miR-223, miR-98 and miR-206 in lung. [score:1]
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[+] score: 17
Third, we compared the total expression levels of pri-let-7b, pri-let-7c-1, pri-let-7f-1, pri-let-7i and pri-mir-98 between the FSL and FRL PFC; none of those pri-let-7 transcripts showed different expression between the rat strains (P>0.5, Figure 1d), indicating that reduction in mature let-7 expression in the FSL did not originate from decreased levels of pri-let-7 transcripts. [score:6]
Second, we examined whether the Il6 reduction in the FSL runners associated with upregulation of let-7 miRNAs that showed a difference between naïve FSL and FRL (let-7b, let-7c, let-7f, let-7i and miR-98). [score:4]
Third, we examined whether increased let-7i and miR-98 in FSL-runners associated with an upregulation of pri-let-7i and pri-mir-98 transcripts. [score:4]
Specifically, let-7b, let-7c, let-7f, let-7i and miR-98 were significantly reduced in FSL (P=0.011, P=0.024, P=0.021, P=0.004 and P=0.006, respectively, Figure 1b). [score:1]
Pri-let-7i levels were significantly increased in the FSL-running group, and pri-mir-98 levels displayed a tendency for increased levels in the FSL-runners (P=0.004 and P=0.093 respectively, Figure 2c). [score:1]
[20] In human, the let-7 family consists of 12 genes encoding nine distinct miRNAs (let-7a to let-7i and miR-98). [score:1]
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[+] score: 17
On the other hand, prenatal stress also upregulated miR-98 expression, which modulates immune responses through cytokine pathways [81], and was shown to downregulate the production of the proinflammatory cytokine IL-10 in macrophages [82]. [score:9]
Both miR-323 and miR-98 upregulation in brains of prenatally stressed offspring may indicate an altered pro-inflammatory state in the brain. [score:4]
The miRNAs differentially regulated by prenatal stress includes miR-23a (up), miR-129-2 (up), miR-361 (down), let-7f (up), miR-17-5p (down), miR-98 (up), miR-425 (down), miR-345-5p (down), miR-9 (up), miR216-5p (up), miR-667 (up), and miR-505 (down) (Figure 3A). [score:2]
The following miRNAs were analyzed (5′ to 3′): mirR-181 and miR-186 (dams); miR-103, miR-151, miR-323, miR-145, miR-425, miR-98 (newborns). [score:1]
Non-stress groups), as observed by microarray analyses, the following candidates were selected for verification by qRT-PCR analysis: miR-151, miR-145, miR-425 (all down) and miR-103, miR-323, miR-98 (up) (Figure 3C). [score:1]
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[+] score: 14
Similarly, miR-195 (predicted to target BDNF), and let-7b and miR-98 (both predicted to target NGF) have been shown previously in human muscle to increase with aging [45], consistent with our analysis in VO rat muscle. [score:5]
Finally, TargetScan identified the following miRNAs that are conserved in humans as likely to influence NGF transcript levels: let-7b-5p and miR-98-5p and these miRNAs share a common seed sequence (CUACCUCA). [score:3]
Of these, only miR-98-5p exhibited an increase in Sarco mouse gastrocnemius muscle (this analysis was not possible in soleus due to limited tissue). [score:1]
Note that we also saw an increase in miR-98-5p in Sarco mouse muscle, which likely reflects a normal response to denervation. [score:1]
Both let-7b-5p and miR-98-5p were increased significantly in VO rat muscle (Fig.   5c). [score:1]
In contrast to the aforementioned studies in aging muscle, most of the miRNAs studied herein have been examined in the context of experimental denervation, including miR-206 (increases after reinnervation), miR-10a-5p (increases four- to seven-fold with denervation), miR-1 (increases up to 10-fold following denervation and remains elevated after reinnervation), miR-195 (increases up to 10-fold with denervation), miR-21 (increases with denervation), miR-221 (no consistent change), miR-222 (no consistent change), and miR-98 (increases up to 10-fold with denervation) [43, 47, 48]. [score:1]
MicroRNAs predicted to influence neurotrophins: a BDNF (miR-206-3p, miR-10a-5p, miR-1b, miR-195-5p and miR-497-5p), b NT3 (miR-21-5p, miR-222-3p and miR-221-3p), and c NGF (let-7b-5p and miR-98-5p) were quantified by qPCR analysis in YA (n = 8) vs VO (n = 10) rat vastus lateralis muscle and WT (n = 8) vs Sarco (n = 7) gastrocnemius muscle. [score:1]
Finally, for NGF, our analysis revealed an increase in both let-7b-5p and miR-98-5p in VO rat muscle. [score:1]
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[+] score: 12
Treatment Group MiRNA changed Log2 (G/CT) Validated targets 80 kVp/0.1 Gy 2 Low fold change – 80 kVp/0.1 Gy Low signals – – 80 kVp/1 Gy miR-34a 1.55 E2F3, Tagln, INHBB miR-29c −1.02 Tpm1 miR-20b-5p −1.65 – miR-204 −1.39 – 30 kVp/2.5 Gy miR-34a 1.08 E2F3, Tagln, INHBB miR-20b-5p −1.55 – miR-98 −1.16 – miR-127 2.08 – The elevated expression of miR-34a was interesting to us, and we decided to proceed with identifying protein levels of its targets E2F3 and transgelin as well as p53, the key protein in DNA damage response. [score:7]
Treatment Group MiRNA changed Log2 (G/CT) Validated targets 80 kVp/0.1 Gy 2 Low fold change – 80 kVp/0.1 Gy Low signals – – 80 kVp/1 Gy miR-34a 1.55 E2F3, Tagln, INHBB miR-29c −1.02 Tpm1 miR-20b-5p −1.65 – miR-204 −1.39 – 30 kVp/2.5 Gy miR-34a 1.08 E2F3, Tagln, INHBB miR-20b-5p −1.55 – miR-98 −1.16 – miR-127 2.08 – Relative miR expression values are represented in folds in the irradiated cells in comparison to non-irradiated control cells as analyzed by miRNA microarray. [score:5]
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[+] score: 12
The top 10 miRNAs upregulated and downregulated upon treatment with Tg and Tm, respectively are shown in Figure 2B-C. The expression of miR-98, let-7d*, miR-374, miR-181d, miR-352, miR-7a and miR-26b were increased both by Tg and Tm in H9c2 cells. [score:9]
Further we found that expression of four miRNAs (miR-20a, miR-98, miR-107 and miR-126) showed a trend similar to that observed in microarray but was not statistically significant (Figure 3). [score:3]
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[+] score: 11
Moreover, miR-98 upregulation could be used as a molecular marker for the colon in active UC patients and was associated with the progression of colitis in UC [10]. [score:4]
The upregulated miRNAs in the colon tissues of UC rats changed by HM were miR-149-5p, miR-351-5p, let-7d-5p, miR-98-5p, let-7a-5p, miR-3559-5p, let-7f-1-3p, miR-3596b, miR-224-5p, miR-411-3p, miR-184, miR-26b-3p, and miR-92b-3p. [score:4]
Our study showed that miR-98 expression showed a decreasing trend in DSS -induced UC colon tissues that could be reversed by HM. [score:3]
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[+] score: 11
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-16-1, hsa-mir-17, hsa-mir-18a, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-20a, hsa-mir-22, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-98, hsa-mir-101-1, hsa-mir-16-2, mmu-let-7g, mmu-let-7i, mmu-mir-1a-1, mmu-mir-15b, mmu-mir-101a, mmu-mir-126a, mmu-mir-130a, mmu-mir-133a-1, mmu-mir-142a, mmu-mir-181a-2, mmu-mir-194-1, hsa-mir-208a, hsa-mir-30c-2, mmu-mir-122, mmu-mir-143, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-181a-1, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-15b, hsa-mir-122, hsa-mir-130a, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-142, hsa-mir-143, hsa-mir-126, hsa-mir-194-1, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-208a, 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-16-1, mmu-mir-16-2, mmu-mir-18a, mmu-mir-20a, mmu-mir-22, mmu-mir-26a-1, mmu-mir-26b, mmu-mir-29c, mmu-mir-98, mmu-mir-326, rno-mir-326, rno-let-7d, rno-mir-20a, rno-mir-101b, mmu-mir-101b, hsa-mir-1-1, mmu-mir-1a-2, hsa-mir-181b-2, mmu-mir-17, mmu-mir-19a, mmu-mir-181a-1, mmu-mir-26a-2, mmu-mir-19b-1, mmu-mir-181b-1, mmu-mir-181c, hsa-mir-194-2, mmu-mir-194-2, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-101-2, hsa-mir-26a-2, hsa-mir-378a, mmu-mir-378a, hsa-mir-326, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, mmu-mir-181b-2, 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-18a, rno-mir-19b-1, rno-mir-19a, rno-mir-22, rno-mir-26a, rno-mir-26b, rno-mir-29c-1, rno-mir-30c-1, rno-mir-30c-2, rno-mir-101a, rno-mir-122, rno-mir-126a, rno-mir-130a, rno-mir-133a, rno-mir-142, rno-mir-143, rno-mir-181c, rno-mir-181a-2, rno-mir-181b-1, rno-mir-181b-2, rno-mir-194-1, rno-mir-194-2, rno-mir-208a, rno-mir-181a-1, hsa-mir-423, hsa-mir-18b, hsa-mir-20b, hsa-mir-451a, mmu-mir-451a, rno-mir-451, ssc-mir-122, ssc-mir-15b, ssc-mir-181b-2, ssc-mir-19a, ssc-mir-20a, ssc-mir-26a, ssc-mir-326, ssc-mir-181c, ssc-let-7c, ssc-let-7f-1, ssc-let-7i, ssc-mir-18a, ssc-mir-29c, ssc-mir-30c-2, hsa-mir-484, hsa-mir-181d, hsa-mir-499a, rno-mir-1, rno-mir-133b, mmu-mir-484, mmu-mir-20b, rno-mir-20b, rno-mir-378a, rno-mir-499, hsa-mir-378d-2, mmu-mir-423, mmu-mir-499, mmu-mir-181d, mmu-mir-18b, mmu-mir-208b, hsa-mir-208b, rno-mir-17-2, rno-mir-181d, rno-mir-423, rno-mir-484, mmu-mir-1b, ssc-mir-15a, ssc-mir-16-2, ssc-mir-16-1, ssc-mir-17, ssc-mir-130a, ssc-mir-101-1, ssc-mir-101-2, ssc-mir-133a-1, ssc-mir-1, ssc-mir-181a-1, ssc-let-7a-1, ssc-let-7e, ssc-let-7g, ssc-mir-378-1, ssc-mir-133b, ssc-mir-499, ssc-mir-143, ssc-mir-423, ssc-mir-181a-2, ssc-mir-181b-1, ssc-mir-181d, ssc-mir-98, ssc-mir-208b, ssc-mir-142, ssc-mir-19b-1, hsa-mir-378b, ssc-mir-22, rno-mir-126b, rno-mir-208b, rno-mir-133c, hsa-mir-378c, ssc-mir-194b, ssc-mir-133a-2, ssc-mir-484, ssc-mir-30c-1, ssc-mir-126, ssc-mir-378-2, ssc-mir-451, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, mmu-mir-378b, mmu-mir-101c, hsa-mir-451b, hsa-mir-499b, ssc-let-7a-2, ssc-mir-18b, hsa-mir-378j, rno-mir-378b, mmu-mir-133c, mmu-let-7j, mmu-mir-378c, mmu-mir-378d, mmu-mir-451b, ssc-let-7d, ssc-let-7f-2, ssc-mir-20b-1, ssc-mir-20b-2, ssc-mir-194a, mmu-let-7k, mmu-mir-126b, mmu-mir-142b, rno-let-7g, rno-mir-15a, ssc-mir-378b, rno-mir-29c-2, rno-mir-1b, ssc-mir-26b
let-7, miR-98, miR-130a and miR-16 showed uniform levels of expression in 13 different tissues but were hardly detected in pancreas (Figure 3A). [score:3]
Similarly, let-7, miR-98, miR-16 and miR-130a are abundantly expressed in 13 of the 14 tissues (except in pancreas) (Figure 3A). [score:3]
Additionally, many other miRNAs, such as let-7, miR-98, miR-16, miR22, miR-26b, miR-29c, miR-30c and miR126, were also expressed abundantly in thymus (Figure 3). [score:3]
miR-98 is represented by 5 reads in our sequences (Table 2). [score:1]
The miR-98 sequence differs from that of the let-7 family by one nt at position 11 from the 5' end, thus miR-98 is also a member of the let-7 family. [score:1]
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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: 5
The TGFBR1 gene, which mediates the action of TGF-β, is a predicted target gene of the let-7/miR-98 family according to TargetScan 4.2 (containing conserved sites for let-7a-g and i, and for miR-98). [score:5]
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[+] score: 4
SCs proliferation and migration were specifically regulated by let-7d/mir-98 through targeting NGF in vitro and in vivo. [score:4]
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[+] score: 4
In fact, these autophagy linked genes’ mRNA includes, the target sequence for miRNAs related to diverse families 5, 6. The gene networks regulating autophagy pathway were determined using a system biology and unrevealed miR-130, miR-98, miR-124, miR-204, and miR-142 as presumed posttranscriptional modulators of this pathway at different levels [6]. [score:4]
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[+] score: 4
Furthermore, among these miRNAs, many were found to be involved in angiogenesis, including several with a regulatory function in cell proliferation, the expression of growth factors and extracellular proteolysis, such as miR-497, miR-98, miR-181a, miR-145, miR-29b and miR-27a 24– 29. [score:4]
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[+] score: 4
Overall, we speculate that microRNAs like miR-15b and miR-98 co-ordinate the regulation of the expression of E-cadherin, ZEB1 (TCF8), HMGA2 and SNAIL. [score:4]
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[+] score: 4
Recent studies revealed that miR-19b, miR-30a, miR-301a promoted the progression of periodontitis [4] and miR-146a, miR-98 were upregulated to contribute to the progression of OA [10]. [score:4]
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[+] score: 3
Additional miRNAs involved in the regulation of the AhR include has-mir-26a-5p, hsa-mir-130b-3p, has-mir-124-3p, has-miR-625-5p and has-miR-98-5p with proven experimental evidence for their participation in the regulation of genes coding for lipid transport most notable CD36, fatty acid binding proteins FABP1, FAB6, FAB7, low density lipoprotein receptor, RXRß and others based on miRTarBase data analysis and PubMed searches. [score:3]
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[+] score: 3
Jones et al. found that mir-9 and mir-98 were identified to be overexpressed in human osteoarthritic tissue [14]. [score:3]
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[+] score: 2
MiR-98, miR-124, miR-130, miR-142, and miR-204, might regulate autophagy [25, 26]. [score:2]
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[+] score: 2
The results of miRror2.0 for the input of mmu miR-98, mmu miR-124, mmu miR-153 and mmu miR-361 are shown. [score:1]
Figure 2A shows the difference in the mapping of the four selected mouse miRNAs (mmu-miR-124, mmu-miR-153, mmu-miR-361 and mmu-miR-98; only four miRNAs were selected for simplicity). [score:1]
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[+] score: 2
The following miRNAs, also present in the VTMs list of Fig 5, were found by RT-PCR to be dysregulated in mouse lung tissue: miR-21, miR-146, miR-20, miR-302, miR-19, miR-98, let-7a, miR-15a. [score:2]
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[+] score: 1
Other miRNAs from this paper: rno-mir-34a, rno-mir-146a, rno-mir-187, rno-mir-155
MicroRNA-98 negatively regulates IL-10 production and endotoxin tolerance in macrophages after LPS stimulation. [score:1]
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[+] score: 1
Other miRNAs from this paper: rno-let-7b, rno-mir-21, rno-mir-132, rno-mir-138-2, rno-mir-138-1
Three studies, including ours identified an increase in mir21, and a decrease in miR98. [score:1]
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[+] score: 1
Significantly, in a previously published study from Arroyo et al. 18 Let-7a and miR-98 were found enriched in the vesicle-enriched and in the vesicle -depleted fractions of the serum respectively. [score:1]
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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-30b, rno-mir-30d, rno-mir-30a, rno-mir-30c-2, rno-mir-33, 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
By the same method, we found that MRAK081523 and Plxna4 had the same MREs for miR-218, miR-141, miR-98 and let-7. Plxna4 reportedly promotes tumour progression and tumour angiogenesis by enhancing VEGF and basic fibroblast growth factor signalling [44]. [score:1]
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Changes in levels of exosomal-miR-98 were not analyzed since miR-98 was not detectable in exosomes secreted by control primary hepatocytes (data not shown). [score:1]
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Other known colon cancer miRNA signatures were confirmed, such as an increase in miR-21 and a decrease in miR-98, but no concordance was observed for these miRNAs and KLF4 (data not shown). [score:1]
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In mice, 12 genes encode members of the Let-7 family, which includes nine slightly different miRNAs (Let-7a, Let-c, and Let-7f [all encoded by two genes], and Let-7b, Let-7d, Let-7e, Let-7g, Let-7i, and miR-98 [all encoded by one gene]). [score:1]
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