sort by

41 publications mentioning rno-mir-24-1

Open access articles that are associated with the species Rattus norvegicus and mention the gene name mir-24-1. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 204
Fig. 8 Under oxidative stress, RIPC -treated rats secrete a considerable number of exosomes, which could be taken up by cardiomyocytes, and miR-24 contained in RIPC-EXO inhibits cardiomyocyte apoptosis by downregulating the expression of Bim, thereby resulting in cardiac protection Under oxidative stress, RIPC -treated rats secrete a considerable number of exosomes, which could be taken up by cardiomyocytes, and miR-24 contained in RIPC-EXO inhibits cardiomyocyte apoptosis by downregulating the expression of Bim, thereby resulting in cardiac protection To detect the number of apoptotic cardiomyocytes, rat hearts were removed 1 day after I/R. [score:15]
In our study, we found that the expression levels of miR-24 in H9c2 cells were significantly increased after pre-incubation with the exosomes isolated from rats that had been subjected to RIPC and that the mechanism by which miR-24 protected the heart from injury was related to the downregulation of Bim expression. [score:8]
Our results also showed that the expression of miR-24 in the exosomes from rat plasma was significantly increased after RIPC and that miR-24 in RIPC-EXO potentially played an important role in cardioprotection by attenuating cardiomyocyte apoptosis through the downregulation of Bim expression. [score:8]
Fig. 8 Under oxidative stress, RIPC -treated rats secrete a considerable number of exosomes, which could be taken up by cardiomyocytes, and miR-24 contained in RIPC-EXO inhibits cardiomyocyte apoptosis by downregulating the expression of Bim, thereby resulting in cardiac protection To detect the number of apoptotic cardiomyocytes, rat hearts were removed 1 day after I/R. [score:8]
Additionally, miR-24 was significantly downregulated in H9c2 cells treated with H [2]O [2] (Fig.   5d) and was upregulated after pre-incubation with RIPC-EXO. [score:7]
Previous studies have demonstrated that miR-24 plays a cardioprotective role in myocardial infarction by downregulating the expression of the pro-apoptotic protein Bim. [score:6]
In conclusion, exosomes derived from the plasma of rats subjected to RIPC could be involved in cardiac protection against IRI via miR-24, which reduces myocardial cell apoptosis by downregulating Bim expression. [score:6]
Based on these observations, we proposed the hypothesis that RIPC-EXO transport miR-24 to cardiomyocytes to attenuate myocardial IRI by decreasing myocardial apoptosis via the downregulation of Bim expression. [score:6]
In conclusion, exosomes induced by RIPC reduced myocardial cell apoptosis resulting from I/R injury by transporting miR-24 into the myocardial cells, in which miR-24 downregulated Bim expression (Fig. 8). [score:6]
As shown in Fig.   4f, Bim was significantly upregulated in H9c2 cells treated with H [2]O [2], and Bim levels were further increased in H9c2 cells in the presence of the miR-24 inhibitor but decreased in H9c2 cells in the presence of the miR-24 mimic. [score:6]
Previous studies have shown that miR-24 can downregulate Bim expression in mice to reduce myocardial cell apoptosis during myocardial infarction [32]. [score:6]
e, f Immunoblot analysis for the expression of Bim and cleaved caspase 3 in H [2]O [2] -treated (100 μM, 6 h) H9c2 cells that had been treated with miR-24 mimics or inhibitors (* P > 0.05, ** P>0.05, [#] P < 0.05, [##] P<0.05, n = 3) Anti-apoptotic effects of RIPC-EXO on H9c2 cells treated with H [2]O [2]To determine the effects of RIPC-EXO harbouring miR-24 on H9c2 cells apoptosis induced by oxidative stress, we pretreated H9c2 cells with phosphate-buffered saline (PBS), EXO or RIPC-EXO, and subjected them to acute H [2]O [2] or vehicle treatment, followed by the determination of apoptotic rates using flow cytometry. [score:5]
e, f Immunoblot analysis for the expression of Bim and cleaved caspase 3 in H [2]O [2] -treated (100 μM, 6 h) H9c2 cells that had been treated with miR-24 mimics or inhibitors (* P > 0.05, ** P>0.05, [#] P < 0.05, [##] P<0.05, n = 3) To determine the effects of RIPC-EXO harbouring miR-24 on H9c2 cells apoptosis induced by oxidative stress, we pretreated H9c2 cells with phosphate-buffered saline (PBS), EXO or RIPC-EXO, and subjected them to acute H [2]O [2] or vehicle treatment, followed by the determination of apoptotic rates using flow cytometry. [score:5]
e, f Immunoblot analysis for the expression of Bim and cleaved caspase 3 in H [2]O [2] -treated (100 μM, 6 h) H9c2 cells that had been treated with miR-24 mimics or inhibitors (* P > 0.05, ** P>0.05, [#] P < 0.05, [##] P<0.05, n = 3) a qPCR analysis of principal miRNAs that have been reported in exosomes from sham-operated and RIPC -treated rats. [score:5]
The miR-24 mimic and mimic-NC were used at a concentration of 50 nM, whereas the miR-24 inhibitor and inhibitor-NC were used at 100 nM. [score:5]
The H9c2 cells were assigned to the following six groups: group 1 (control); group 2 (H [2]O [2] -treated); group 3 (H [2]O [2] + EXO); group 4 (H [2]O [2] + RIPC-EXO); group 5 (H [2]O [2] + RIPC-EXO + miR-24 inhibitor); and group 6 (H [2]O [2] + RIPC-EXO + miR-24 inhibit-NC). [score:5]
Therefore, RIPC-EXO may reduce apoptosis in H [2]O [2] -treated H9c2 cells by delivering miR-24 to these cells to negatively regulate Bim expression. [score:4]
Nine miRNAs (miR-21, miR-24, miR-214, miR-132, miR-195, miR-210, miR-144, miR-150 and miR-34a) were found in exosomes obtained from rats subjected to RIPC, but only miR-24 was significantly upregulated ([#] P < 0.05, n = 4). [score:4]
To demonstrate whether miR-24 can reduce apoptosis in cardiomyocytes, we performed gain- and loss-of-function experiments using miR-24 mimics/inhibitors. [score:3]
Fig. 4 a qRT-PCR analysis of miR-24 level in H9c2 cardiomyoblasts transfected with miR-24 mimics or inhibitors or respective NC RNAs (* P > 0.05, ** P>0.05, [#] P < 0.05, [ ##] P<0.05, n = 4). [score:3]
We observed that the expression of miR-24 was significantly higher in exosomes from the plasma of rats subjected to RIPC that in those from rats subjected to sham operation in vivo. [score:3]
Interestingly, we found that the expression level of miR-24 was to be significantly altered. [score:3]
RIPC -induced expression of miR-24 in exosomes. [score:3]
However, the addition of the miR-24 inhibitor counteracted the effect of RIPC-EXO -induced reduction in apoptosis. [score:3]
e Representative confocal microscopy images of H9c2 cells incubated with exosomes from H9c2 cells that had been transfected with FAM -labelled miR-24 mimics (unlabelled miRNAs were used as controls) a qRT-PCR analysis of miR-24 level in H9c2 cardiomyoblasts transfected with miR-24 mimics or inhibitors or respective NC RNAs (* P > 0.05, ** P>0.05, [#] P < 0.05, [ ##] P<0.05, n = 4). [score:3]
The RIPC-EXO -treated H9c2 cells had an approximately eightfold higher expression of miR-24 than did the EXO -treated cells (Fig.   5d). [score:3]
Correspondingly, the addition of the miR-24 inhibitor counteracted the apoptosis-reducing effect of RIPC-EXO (Supplemental Fig.   IC-D). [score:3]
d Relative LDH activity in the culture media of H9c2 cells transfected with miR-24 mimics or inhibitors or respective NC RNAs (* P > 0.05,** P>0.05, [#] P < 0.05, [##] P<0.05 n = 5). [score:3]
Since Bim has been shown to be involved in oxidative stress -induced cell death [26], by evaluating the expression levels of Bim in H [2]O [2] -treated H9c2 cells in the presence of the miR-24 inhibitor or miR-24 mimic via western blotting, we next investigated whether Bim is a target of miR-24 in H9c2 cells. [score:3]
d Exosomes were isolated from RIPC -treated rat plasma and incubated with the indicated reagents, after which RNA was isolated, and the expression levels of miR-24 were determined using qPCR (* P > 0.05, [#] P < 0.05, n = 3). [score:3]
The importance of miR-24 in cardioprotection was further supported by the finding that the addition of the miR-24 antagomir could counteract the miR-24 -induced suppression of apoptosis. [score:3]
b, c Flow cytometric analysis of apoptosis of H [2]O [2]-exposed (100 μM, 6 h) H9c2 cells treated with miR-24 mimics or inhibitors (* P > 0.05, ** P>0.05, [#] P < 0.05, [##] P<0.05, n = 4). [score:3]
In addition, the miR-24 mimic significantly decreased the levels of cleaved caspase 3, however, the miR-24 inhibitor increased these levels (Fig.   4e) in H9c2 cells treated with 100 μM H [2]O [2]. [score:3]
b, c Flow cytometric analysis of the uptake of exosomes by H9c2 cells at various time points We further determined the expression of nine miRNAs (miR-24, miR-21, miR-214, miR-132, miR-195, miR-210, miR-144, miR-150 and miR-34a) in both RIPC-EXO and EXO (Fig.   3a). [score:3]
b Study design for systemic delivery of RIPC-EXO in the rat I/R mo del H9c2 cells were exposed to 100 µM H [2]O [2] for 6 h in the presence or absence of RIPC-EXO or H9c2 cells transfected with the miR-24 inhibitor or mimic. [score:3]
The miR-24 mimic, inhibitor and NC RNAs (RiboBio, Guangzhou, China) were transfected into cells with Lipofectamine 3000 (Life Technologies) according to the manufacturer’s instructions. [score:3]
Qian L miR-24 inhibits apoptosis and represses Bim in mouse cardiomyocytesJ. [score:3]
The expression level of miR-24 was analysed in the border zone and distant zone of hearts 24 h after I/R induction or sham surgery. [score:3]
As shown in Fig.   4b, c, the percentage of apoptotic cells was decreased in H9c2 cells treated with the miR-24 mimic but was increased in H9c2 cells treated with the miR-24 inhibitor. [score:3]
Additionally, the expression level of miR-24 was detected by real-time PCR (RT-PCR), indeed, miR-24 was successfully transfected into the H9c2 cells (Fig.   4a). [score:3]
First, miR-24 mimics or inhibitors were transfected into H9c2 cells, and the transfection efficiency was assessed using fluorescence microscopy (Supplemental Fig.   IF). [score:3]
The expression levels of miR-24 in the border zone of the I/R group was lower than that in the sham group, but there was no significant statistical difference between the two groups in the distant zone. [score:3]
Consistent with the above observations, lactate dehydrogenase (LDH) assays showed that the miR-24 mimic decreased LDH release, whereas miR-24 inhibitors had the opposite effects (Fig.   4d). [score:2]
Among these miRNAs, miR-24 level was significantly higher in RIPC-EXO than in EXO purified from sham-operated rat plasma (Fig.   3b). [score:1]
As expected, the addition of the miR-24 antagomir counteracted RIPC-EXO -induced reduction in apoptosis. [score:1]
Potential involvement of miR-24 in RIPC-EXO in protecting cardiomyocytes against apoptosis. [score:1]
The rats were assigned to six groups based on the injection as follows: group 1 (PBS + sham), intramyocardial delivery of 10 µl PBS to sham rat; group 2 (PBS + I/R), intramyocardial delivery of 10 µl PBS to I/R rat; group 3 (EXO + I/R), intramyocardial delivery of 10 µl exosomes purified from the plasma from sham-operated rats; group 4 (RIPC-EXO + I/R), intramyocardial delivery of 10 µl exosomes purified from the plasma of RIPC -treated rats; group 5 (RIPC-EXO + I/R + miR-24 antagomir), intramyocardial delivery of 10 µl exosomes purified from the plasma of RIPC -treated rats and 10 nmol of the miR-24 antagomir; and group 6 (RIPC-EXO + I/R + miR-24 antagomir control). [score:1]
However, the levels of miR-24 in the RIPC-EXO + I/R group were higher than those in the I/R group in the border zone (Supplemental Fig.   IIA-B). [score:1]
b Levels of miR-24 in exosomes and exosome-free plasma before and after RIPC were determined by RT-PCR (* P > 0.05, [#] P < 0.05, n = 4). [score:1]
To demonstrate that exosomes were able to transport miR-24 to recipient cells, we fluorescently labelled miR-24 mimics and transfected them into cells, collected the exosomes secreted by the cells, and then incubated H9c2 cells with these exosomes. [score:1]
Anti-apoptotic effects of miR-24 in vitro. [score:1]
Indeed, miR-24 detected in plasma was mainly harboured within exosomes (Fig.   3d). [score:1]
Collectively, these findings demonstrated that miR-24 had anti-apoptotic function under conditions of oxidative stress. [score:1]
We found that H9c2 cells harboured fluorescently labelled miR-24 mimics (Fig.   3e). [score:1]
Guo C Deng Y Liu J Qian L Cardiomyocyte-specific role of miR-24 in promoting cell survivalJ. [score:1]
The level of miR-24 in the exosomes was significantly decreased only after the addition of RNase and the cell membrane-disrupting agent, indicating that most of the miR-24 molecules were present in plasma exosomes. [score:1]
Since the subject of our study was IRI, we selected nine miRNAs that have been reported to be involved either in oxidative stress (such as miR-150 and miR-21) 14, 15 or in cardiomyocyte apoptosis (such as miR-195, miR-132, miR-140, miR-144, miR-24, miR-214 and miR-34a) 16– 21 in our investigation and, using quantitative PCR (qPCR), explored whether RIPC could modify the expression level of these nine miRNAs in plasma exosomes. [score:1]
d qRT-PCR analysis of miR-24 levels in H9c2 cells from the various groups (* P > 0.05,** P>0.05, [#] P < 0.05, [##] P<0.05, n = 3). [score:1]
[1 to 20 of 58 sentences]
2
[+] score: 137
Over-Expression of miR-24 Suppressed the Expression of Wnt4 Signaling Pathway. [score:7]
Interestingly, up-regulation of miR-24 could not only reduce gene expressions (Figure 5B, n = 6) but significantly reduce the levels of proteins by 36.07%, 34.67%, and 31.06%, respectively, in balloon-injured carotid arteries (Figure 5C–F, n = 6). [score:6]
In summary, we have shown that miR-24 adenoviral transfection could attenuate VSMC proliferation and neointimal hyperplasia in the diabetic rats after vascular injury by regulating the expressions of Cyclin D1 and p21 through inhibition of the Wnt4 signaling pathway. [score:6]
Over-Expression of miR-24 Suppressed Neointimal Hyperplasia in Diabetic Rats. [score:5]
Wnt4 has been predicted as a potential target gene of miR-24 with TargetScan software (Figure 5A) [19]. [score:5]
One week before surgery, the 48 STZ -induced diabetic rats (350–400 g) were assigned into four groups randomly and equally: sham group (n = 12); carotid artery balloon injury with phosphate buffered saline treatment group (PBS group; n = 12); carotid artery balloon injury transfected with adenovirus expressing Scramble-GFP group (Ad-Scramble group; n = 12); and carotid artery balloon injury transfected with adenovirus expressing miR-24-GFP group (Ad-miR-24 group; n = 12). [score:5]
In fact, Wnt4 has been predicted as a potential target gene of miR-24 by the bioinformatics of TargetScan. [score:5]
miR-24 is a VSMC-enriched microRNA and it has several target genes in VSMCs predicted by TargetScan. [score:5]
Interestingly, transfection with adenoviral over -expression of miR-24 into a balloon-injured carotid artery markedly increased miR-24 expression (adenovirus (Ad-miR-24) group vs. [score:5]
The AdMax system (Microbix Biosystems, Toronto, ON, Canada) was used to generate the adenovirus expressing miR-24 (Ad-miR-24-GFP) or expressing Scramble (Ad-Scramble-GFP). [score:5]
Interestingly, over -expression of miR-24 significantly inhibited the gene and protein levels of Cyclin D1 but increased the levels of p21 (vs. [score:5]
The Wnt4 gene plays a pivotal role in vascular occlusive disease and our current data suggest that miR-24 may ease this effect by reducing Wnt4 expression. [score:5]
Over-Expression of miR-24 Altered the Expression of Cell Cycle-Associated Molecules. [score:5]
Over-Expression of miR-24 Inhibited VSMC Proliferation in Diabetic Rats. [score:5]
In this present study, we found that miR-24 was significantly down-regulated in diabetic rat carotid arteries after a balloon injury at 14 days. [score:4]
Briefly, β-catenin sharply increased in diabetic rats’ carotid arteries after a balloon injury, but it was reduced after up-regulation of miR-24. [score:4]
Thus, miR-24 may constitute a new therapeutic target for vascular RS. [score:3]
Our results also indicated that this anti-proliferative effect of miR-24 occurred via the suppression of the Wnt4 signaling pathway. [score:3]
Salvi A. Abeni E. Portolani N. Barlati S. de Petro G. Human hepatocellular carcinoma cell-specific miRNAs reveal the differential expression of miR-24 and miR-27a in cirrhotic/non-cirrhotic HCC Int. [score:3]
In this study, our experiments confirmed that the expressions of miR-24 and Wnt4 were inversely correlated in diabetic rat carotid arteries. [score:3]
Additionally, we demonstrated that over -expression of miR-24 could ease neointimal hyperplasia through its anti-proliferative effect on VSMCs. [score:3]
In this study, we find that over -expression miR-24 by adenoviral transfection could reduce neointimal hyperplasia significantly in the injured carotid arteries of diabetic rats. [score:3]
miR-24 expression was examined both in uninjured and injured carotid arteries in diabetic rats. [score:3]
Over -expression of miR-24 reduced VSMC proliferation and neointimal hyperplasia in diabetic rats after vascular injury. [score:3]
2.2. miR-24 Expression Was Decreased in Carotid Artery after Balloon Injury in Diabetic Rats. [score:3]
Construction of miR-24 Expression Adenoviral Vector. [score:3]
In addition, our unpublished data has suggested that miR-24 is VSMC-enriched, but has low expression in endothelial cells (ECs). [score:3]
In this study, we (1) observe the changes in miR-24 in diabetic rat carotid arteries after a balloon injury; (2) determine if over -expression of miR-24 could attenuate VSMC proliferation and neointimal hyperplasia in vivo; (3) seek a better understanding of the underlying mechanism of miR-24 involved in these biological processes. [score:3]
Recently, Chan et al. also indicated that miR-24 could regulate the VSMC phenotype through the platelet derived growth factor (PDGF) and transforming growth factor-β (TGF-β) pathways [22]. [score:2]
To sum up, the above research results demonstrated that miR-24 may be involved in the formation of neointimal hyperplasia and vascular RS by regulating the functional state of VSMCs instead of ECs. [score:2]
MiR-24 is a type of tumor-suppressing microRNAs [21]. [score:2]
The delivery of miR-24 into diabetic rat carotid arteries via recombinant adenovirus vector is done to alleviate VSMC proliferation and neointimal hyperplasia and is just one type of gene therapy used in our present study. [score:1]
We delivered miR-24 into rat carotid arteries successfully with the adenoviral vector -mediated transfection system. [score:1]
Thus, we presume that miR-24 would be involved in the neointimal hyperplasia and it may have an anti-proliferative effect on VSMCs. [score:1]
For adenovirus transduction, a 100 μL solution of Ad-Scramble (1 × 10 [9] PFU/mL), Ad-miR-24 (1 × 10 [9] PFU/mL) or PBS was infused into the injured common carotid artery segment and incubated for approximately 30 min. [score:1]
miR-24 is VSMC-enriched and our unpublished data also indicated that the effect of miR-24 is mainly due to VSMCs, but not ECs, which may be a huge advantage of using miR-24 to reduce RS. [score:1]
However, the role of miR-24 in the neointimal formation of the diabetic rat after vascular injury remains unclear. [score:1]
To demonstrate the efficiency of adenovirus delivery into the carotid artery, Ad-Scramble and Ad-miR-24 were both labeled with GFP. [score:1]
The intima/media ratio was also markedly less in Ad-miR-24 transfected arteries (0.696 ± 0.056) than in Ad-Scramble transfected (1.702 ± 0.126, [#] p < 0.05, vs. [score:1]
Ad-miR-24 group) and PBS treated arteries (1.711 ± 0.131, [#] p < 0.05, vs. [score:1]
In brief, the precursor DNA of Rno-miR-24 (MI0000298) was synthesized by Genechem (Shanghai, China). [score:1]
To further analyze the exact mechanisms by which miR-24 inhibited VSMC proliferation and neointimal hyperplasia in the diabetic rats after vascular injury, the mRNA and protein levels of cell cycle -associated molecules were measured by Western blotting and qRT-PCR. [score:1]
The underlying mechanism of the anti-proliferative effects of miR-24 was associated with the Wnt4/β-catenin signaling pathway. [score:1]
Ad-miR-24 group) (Figure 3D, n = 6). [score:1]
[1 to 20 of 44 sentences]
3
[+] score: 46
As MIR24-1 is linked to 5 genes that are upregulated in response to LTP, the prediction from this network analysis is that MIR24-1 is downregulated in response to LTP, thus allowing the expression of a subset of linked genes. [score:9]
This resulted in the identification of 30 genes that were predicted to be targeted by MIR34a and 19 genes predicted to be targeted by MIR24-1 (Table S7 and S8). [score:5]
Furthermore, as a number of the differentially expressed genes (e. g. FOXO1, NUMBL, MIR24-1) or molecules predicted by the IPA software (e. g. MIR124) have reported roles in neurogenesis these highlight a potential role of gene expression in LTP-stimulated neurogenesis. [score:5]
Table S8 Targets of miR-24-1 predicted by TargetScan, miRanda and PicTar. [score:5]
Prediction of MIR24-1 targets revealed 329 genes according to TargetScan, 386 according to miRanda, and 369 according to PicTar. [score:5]
We tested this hypothesis using TaqMan microRNA qPCR and found a significant downregulation of MIR34A (0.53 ± 0.16 (average ± S. E. M), n = 5, p<0.05 two-tailed t-test) and MIR24-1 (0.59 ± 0.12, n = 9, p<0.05 two-tailed t-test) 5 h post-LTP (Figure 8). [score:4]
This does not discount the involvement of these microRNA in LTP consolidation but predicts that MIR34a and MIR24-1 at least contribute to LTP consolidation at the level of translational repression. [score:3]
However, when we screened our LTP datasets (5 h or 24 h) for the algorithm-predicted MIR34a and MIR24-1 target genes, we found no crossover between the groups. [score:3]
To investigate the potential mRNA targets of MIR34a and MIR24-1 we used the algorithms TargetScan, PicTar and miRanda. [score:3]
Potentially, as antagonism of MIR24-1 has been shown to promote cell proliferation [52] and MIR34A regulates neural stem cell differentiation [53], these data suggest microRNA may also regulate LTP-related neurogenesis. [score:3]
In 5 h-Network 2 (Figure 7B; Score 33) the microRNA MIR24-1 formed a hub, while MIR34A is present within 5 h-Network 3 (Figure 7C; Score 18). [score:1]
[1 to 20 of 11 sentences]
4
[+] score: 30
The expression of miR-24 is down-regulated during MI and miR-24 regulates cardiomyoblast apoptosis, in part by direct repression of the BH3-only domain–containing protein Bim [22]. [score:8]
Further ectopic expression of miR-24 in a mouse MI mo del inhibited cardiomyoblast apoptosis, attenuated infarct size, and reduced cardiac dysfunction [22]. [score:5]
The miRNAs (miR-206, miR-24, miR-125b, miR-133b) deregulated upon UPR in H9c2 cells are abundantly expressed in adult heart. [score:4]
We observed that changes in the expression of nine miRNAs (miR-24, miR-25, miR-7a, miR-103, miR-17-5p, miR-106b, miR-93, miR-206 and miR-133b) analyzed by qRT-PCR were consistent with those by miRNA microarray at p < 0.05 (Figure 3). [score:3]
We found that expression of many miRNAs (miR-24, miR-25, miR-7a, miR-103, miR-17-5p, miR-106b, miR-93, miR-206 and miR-133b) changed significantly during conditions of UPR in cardiomyoblasts. [score:3]
The expression of miR-122, miR-93, miR-103, miR-107, miR-206, miR-143, miR-24, and miR-106b were reduced upon treatment with Tg and Tm in H9c2 cells. [score:3]
We found that miRNAs (miR-206, miR-24, miR-125b, miR-133b) with known function in cardiomyoblasts biology [20– 22] were significantly deregulated during the conditions of UPR in H9c2 cells. [score:2]
We found that miRNAs with known function in cardiomyoblasts biology (miR-206, miR-24, miR-125b, miR-133b) were significantly deregulated during the conditions of UPR in H9c2 cells. [score:2]
[1 to 20 of 8 sentences]
5
[+] score: 22
The down-regulated miRNAs included miR-24, miR-26a, miR-126, and Let-7a, b, c, f. The up-regulated miRNAs were composed of miR-344, miR-346, miR-99a, miR-127, miR-128b, miR-135b, and miR-30a/b. [score:7]
Moreover, we found that the down-regulated miRNAs, miR-26a, miR-24, and miR-Let-7abcf family, were inversely related to their predicted mRNA targets, Sod2, and Ebf1. [score:6]
Among the 11 up-regulated mRNAs, Ebf1 (Early B-cell factor 1) was inversely correlated to miR-24. [score:4]
The down-regulated miRNAs included miR-24, miR-26a, miR-126, and Let-7 family members. [score:4]
While Sod2 was inversely correlated with Let-7a, b, c, f., Ebf1 and Apc were inversely correlated with miR-24 and miR-26a, respectively. [score:1]
[1 to 20 of 5 sentences]
6
[+] score: 22
From P4 to P28, miRNAs displayed very similar expression between both progeny: 0–22 (<5%) miRNAs displayed differential expression and 0–7 of them (<2%) had expression differences higher than 3. Ratios of miR-7a-5p, miR-24-3p, miR-29-3p, miR-137-3p or miR-1843-5p expressions relatively to miR-124-3p expression calculated from RT-qPCR at P28 data matched those calculated from HTS data (Fig. 3B). [score:7]
Given the number of miRNAs and the limited quantity of material in individual ARC/MEs, we selected six miRNAs: miR-124a-3p which is wi dely expressed throughout brain 15, miR-29a/b-3p whose brain-specific knockdown results in neuronal cell death 16 17, miR-7a-5p and miR-137-3p which are expressed in hypothalamic nuclei including ARC 18, miR-24-3p and miR-1843-5p which are still poorly or not clearly documented. [score:6]
As the U6 snRNA was excluded from small RNA fractions and could not been used as an internal reference to quantify miRNA expressions, we quantified the expression of miR-7a-5p, miR-24-3p, miR-29-3p, miR-137-3p and miR-1843-5p relatively to that of miR-124-3p, at P4, P8, P14.4 and P21.4 relatively to P28, from RT-qPCR amplification or sequencing data (Fig. 3A). [score:5]
Expression of miR-7a-5p, miR-24-3p, miR-29-3p, miR-137-3p and miR-1843-5p were quantified relatively to those of miR-124-3p, and relatively to those of stage P28, by using the ΔΔCt method 25 and experimentally ascertained amplification efficiencies. [score:3]
Out of the 20 comparisons, RT-qPCR amplification and sequencing data gave similar information exept in the two cases of miR-24-3p at stage P8 and stage P14. [score:1]
[1 to 20 of 5 sentences]
7
[+] score: 21
More importantly, the miRNAs analyzed in this study not only included the miRNAs like Let-7a, miR-15b, miR24, miR-100 and miR-125 which may suppress the expression of cyclins A and B, and miRNAs such as Let-7a, miR24 and miR-125 which may regulate activity of CDK1, but also miRNAs such as miR-181a, miR-221 and miR-222 which can target CDK inhibitors [30– 32]. [score:10]
To investigate whether miRNAs have a role in the cell cycle regulation of splenocytes following aniline exposure, the expression of miRNAs, including Let-7a, miR-15b, miR24, miR-100, miR-125, miR-181a, miR-221 and miR-222 which are known to mainly control G2/M phase regulators [30– 32], was analyzed by using real-time PCR and the results are presented in Fig 7. Aniline exposure led to significantly decreased expression of Let-7a (decreased 82%), miR-15b (decreased 62%), miR24 (decreased 78%), miR-100 (decreased 63%), miR-125 (decreased 86%), whereas miR-181a, miR-221 and miR-222 increased by 155%, 78% and 56%, respectively, in comparison to controls (Fig 7). [score:5]
Therefore, greater decreases in Let-7a, miR-15b, miR24, miR-100 and miR-125 expression and significant increases in miR-181a, miR-221 and miR-222 levels in the spleens following aniline treatment may be mechanistically important in generalizing that aniline exposure leads to increased cyclin A, cyclin B, CDK1, and decreased p21, p27, thus triggering the splenocytes to go through G2/M transition. [score:3]
Real-time PCR analysis of miRNAs Let-7a, miR-15b, miR24, miR-100 and miR-125 (A), and miRNAs miR-181a, miR-221 and miR-222 (B) expression in rat spleens following aniline exposure. [score:3]
[1 to 20 of 4 sentences]
8
[+] score: 21
Therefore, increased expression of miR-29 and miR-24 and reduced expression of miR-34, miR-130 and miR-378 may be responsible for the beneficial effects exerted by MSC-Exo. [score:5]
Importantly, in vivo expression of miR-24 in a mouse MI mo del inhibited cardiomyocyte apoptosis, attenuated infarct size, and reduced cardiac dysfunction [34]. [score:5]
The expression of miR-29 and miR-24, which positively regulate cardiac functions, was relatively high (Figure 3(a)). [score:4]
Upregulation of miR-24 limits aortic vascular inflammation [33]. [score:4]
Our results showed high expression of miR-29 and miR-24 in both MSC-Exo and MSCs. [score:3]
[1 to 20 of 5 sentences]
9
[+] score: 21
24-Hour Acute ZT06 Expression 24-Hour Chronic ZT06 Expression 2-Week chronic ZT06 Expression rno-miR-142-5p Over rno-miR-126a-5p Under rno-miR-146a-5p Under rno-miR-150-5p Over rno-miR-30b-5p Under rno-miR-24-3p Under rno-miR-335 Under rno-let-7b-5p Over rno-miR-130a-3p Over rno-miR-15b-5p Over rno-miR-99a-5p Over rno-miR-127-3p Under rno-miR-133a-3p Under rno-miR-10a-5p Over rno-miR-672-5p Over rno-miR-l-3p Under rno-let-7c-5p Over rno-miR-193-3p Over rno-miR-142-5p Under rno-miR-146b-5p Under rno-miR-150-5p Over Of the three ZT06 groups that illustrated differential expression of miRNAs due to CD, emphasis was placed on the two-week chronic ZT06 group due to the differential expression of miRs 146a and 146b, and miR-127 (Figures 5A-5B and 6A). [score:11]
24-Hour Acute ZT06 Expression 24-Hour Chronic ZT06 Expression 2-Week chronic ZT06 Expression rno-miR-142-5p Over rno-miR-126a-5p Under rno-miR-146a-5p Under rno-miR-150-5p Over rno-miR-30b-5p Under rno-miR-24-3p Under rno-miR-335 Under rno-let-7b-5p Over rno-miR-130a-3p Over rno-miR-15b-5p Over rno-miR-99a-5p Over rno-miR-127-3p Under rno-miR-133a-3p Under rno-miR-10a-5p Over rno-miR-672-5p Over rno-miR-l-3p Under rno-let-7c-5p Over rno-miR-193-3p Over rno-miR-142-5p Under rno-miR-146b-5p Under rno-miR-150-5p Over Differentially expressed miRNAs based on Illumina sequencing in all the circadian-disrupted samples and their links to breast cancer development and circadian rhythms. [score:10]
[1 to 20 of 2 sentences]
10
[+] score: 19
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-16-1, hsa-mir-17, hsa-mir-21, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-30a, hsa-mir-31, hsa-mir-96, hsa-mir-99a, hsa-mir-16-2, hsa-mir-30c-2, hsa-mir-30d, hsa-mir-182, hsa-mir-183, hsa-mir-211, hsa-mir-217, hsa-mir-218-1, hsa-mir-218-2, hsa-mir-221, hsa-mir-222, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-23b, hsa-mir-30b, hsa-mir-125b-1, hsa-mir-132, hsa-mir-143, hsa-mir-145, hsa-mir-191, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-184, hsa-mir-190a, hsa-mir-195, rno-mir-322-1, rno-let-7d, rno-mir-335, rno-mir-342, rno-mir-135b, hsa-mir-30c-1, hsa-mir-299, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-379, hsa-mir-382, hsa-mir-342, hsa-mir-135b, hsa-mir-335, rno-let-7a-1, rno-let-7a-2, rno-let-7b, rno-let-7c-1, rno-let-7c-2, rno-let-7e, rno-let-7f-1, rno-let-7f-2, rno-let-7i, rno-mir-15b, rno-mir-16, rno-mir-17-1, rno-mir-21, rno-mir-23a, rno-mir-23b, rno-mir-24-2, 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
Among the miRNAs examined, 79 miRNAs (24%) responded to the hyperandrogenic condition and interestingly, 80% of which were upregulated compared to the control group supporting the notion that hyperandrogenic condition down-regulates androgen receptors in the granulosa cells [35] which could be mediated by these upregulated miRNAs (rno-miR-379*, rno-let-7d, rno-miR-24, rno-miR-673, rno-miR-26b, rno-miR-335, rno-miR-382*, rno-miR-412, rno-miR-99a*, rno-miR-543, rno-miR-674-3p, rno-miR-409-3p). [score:9]
A list of differentially expressed miRNAs (Fold change ≥ 2 and their corresponding P value) is presented in Figure  4. Beside this group, miRNAs which were also highly abundant in DHT -treated ovaries are rno-miR-221, rno-miR-222, rno-miR-25, rno-miR-26b, rno-miR-379*, rno-let-7d, rno-miR-24, rno-miR-673, rno-miR-26b, rno-miR-335, rno-miR-382*, rno-miR-412, rno-miR-99a*, rno-miR-543, rno-miR-674-3p, rno-miR-409-3p. [score:3]
Among the fourteen miRNAs mapped to the ingenuity databases, twelve (rno-let-7d, rno-miR-132, rno-miR-182, rno-miR-183, rno-miR-184, rno-miR-21, rno-miR-221, rno-miR-24, rno-miR-25, rno-miR-26b, rno-miR-31 and rno-miR-96) had 171 experimentally validated targets. [score:3]
Whereas rno-miR-24 and rno-miR-183 were highly expressed in the theca and, to a lesser extent, in the granulosa cells of the cystic follicles (Figure  5), Rno-miR-31 and rno-miR-96 were present in the cumulus granulosa cells. [score:3]
These included rno-miR-24, rno-miR-31, rno-miR-96, rno-miR-183, rno-miR-222, rno-miR-489, U6 snRNA (positive control) and scrambled miRNA (negative control). [score:1]
[1 to 20 of 5 sentences]
11
[+] score: 14
Other miRNAs from this paper: rno-mir-24-2
To explore the mechanisms that are involved in Bim induction following GCN5 inhibition, we first examined whether CPTH2 treatment can repress the expression of miR-24, a microRNA which is known to negatively regulate Bim expression. [score:8]
[33] Q-PCR results showed that miR-24 levels in the CPTH2 group are not significantly different from those in control (Figure 5a, 0.05< P>0.05), indicating that Bim induction following GCN5 inhibition is not through alteration of miR-24 expression. [score:5]
The qPCR was performed in ABI 7300 Real-Time PCR System (Applied Biosystems, Thermo Fisher Scientific, Waltham, MA, USA) and relative miR-24 expression was calculated using the formula ratio=2 [−ΔΔCt]. [score:1]
[1 to 20 of 3 sentences]
12
[+] score: 13
Among the up-regulated miRNAs, miR-106b, miR-25 and miR-19b share the same primary transcripts, and miR-24 and miR-27 share primary transcripts. [score:4]
Some up-regulated miRNAs such as miR-19a, miR-24 and miR-128a were unchanged at the level of their primary transcripts. [score:4]
Some miRNAs such as miR-24, miR-186, let-7f and miR-320 showed changes in expression throughout all time points (Figure S2C). [score:3]
Among these miRNAs with shared directions of change in in vitro cultured hippocampal neurons and in vivo hippocampal CA1 regions after either neuronal stimulation or contextual conditioning were miR-24, miR-326, miR-320, miR-21 and miR-10b. [score:2]
[1 to 20 of 4 sentences]
13
[+] score: 12
Amplification was performed using a qPCR Thermal Cycler (Applied Biosystems, Nieuwerkerk aan den IJssel, The Netherlands) with a denaturation step at 95 °C for 10 min, followed by 50 cycles of 95 °C for 15 s and 60 °C for 60 s. Data of these qPCR experiments were normalized using the geometric mean [26, 28] of the two uniformly expressed miRNAs, i. e., miR-16 and miR-24. [score:3]
miR-24 and miR-16, surrogate markers for total miRNA expression, were detectable in all samples. [score:3]
The expression profiles of miR-24 and miR-16 have been reported to be stable in several bodily fluids and tissues [24– 27], and were therefore used for normalization purposes. [score:3]
Again, miR-24 and miR-16 were detected in all samples, while the proportion of individuals with undetectable miR-219 was higher in the MS patients’ groups (Fig. 1c). [score:1]
Levels were normalized using the geometric mean of miR-24 and miR-16. [score:1]
Relative expression levels (REL) were calculated using the formula REL = 2 [− ∆Ct], where Ct is cycle threshold, and ∆Ct = Ct (miRNA) –  Ct (geometric mean of miR-16 and miR-24). [score:1]
[1 to 20 of 6 sentences]
14
[+] score: 11
Within the genetic background scanned for miRNA expression on Exiqon arrays, miR-24 and miR-26b were significantly correlated with GH and PRL, with miR-26b being reported to have a potential impact upon expression of the TF Pit-1 in GH3 cells by inhibiting the Pit-1 inhibitor called Lef-1 [59]. [score:9]
We selected the top 9 miRNAs (miR-200a, miR-200b, miR-182, miR-429, miR-183, miR-200c, miR-141, miR-96 and miR-24) showing the highest standard deviations. [score:1]
Of the 9 miRNAs, miR-24 shows the best correlation with GH and PRL (Fig 6C). [score:1]
[1 to 20 of 3 sentences]
15
[+] score: 9
It was reported that IPre up-regulated miR-1, miR-21 and miR-24, and the protein expression of HSP70 was up-regulated by pretreatment of these miRNAs. [score:9]
[1 to 20 of 1 sentences]
16
[+] score: 8
MiR-148-3p, mir-17-5p, miR-181a-5p, miR-19b-3p and miR-24-3p were predicted to control the expression of the following target genes: Interleukin 6 signal transducer IL6ST (gp130). [score:5]
Amongst the 5 miRNAs (miR148-3p, miR17-5p, miR181a-5p, miR19b-3p and miR24-3p) targeting multiple genes from our 70 genes list, mir17-5p, which is increased with stress was confirmed by qRT-PCR. [score:3]
[1 to 20 of 2 sentences]
17
[+] score: 8
Other miRNAs from this paper: mmu-mir-30a, mmu-mir-101a, mmu-mir-125a, mmu-mir-125b-2, mmu-mir-132, mmu-mir-134, mmu-mir-135a-1, mmu-mir-138-2, mmu-mir-142a, mmu-mir-150, mmu-mir-154, mmu-mir-182, mmu-mir-183, mmu-mir-24-1, mmu-mir-194-1, mmu-mir-200b, mmu-mir-122, mmu-mir-296, mmu-mir-21a, mmu-mir-27a, mmu-mir-92a-2, mmu-mir-96, rno-mir-322-1, mmu-mir-322, rno-mir-330, mmu-mir-330, rno-mir-339, mmu-mir-339, rno-mir-342, mmu-mir-342, rno-mir-135b, mmu-mir-135b, mmu-mir-19a, mmu-mir-100, mmu-mir-139, mmu-mir-212, mmu-mir-181a-1, mmu-mir-214, mmu-mir-224, mmu-mir-135a-2, mmu-mir-92a-1, mmu-mir-138-1, mmu-mir-181b-1, mmu-mir-125b-1, mmu-mir-194-2, mmu-mir-377, mmu-mir-383, mmu-mir-181b-2, rno-mir-19a, rno-mir-21, rno-mir-27a, rno-mir-30a, rno-mir-92a-1, rno-mir-92a-2, rno-mir-96, rno-mir-100, rno-mir-101a, rno-mir-122, rno-mir-125a, rno-mir-125b-1, rno-mir-125b-2, rno-mir-132, rno-mir-134, rno-mir-135a, rno-mir-138-2, rno-mir-138-1, rno-mir-139, rno-mir-142, rno-mir-150, rno-mir-154, rno-mir-181b-1, rno-mir-181b-2, rno-mir-183, rno-mir-194-1, rno-mir-194-2, rno-mir-200b, rno-mir-212, rno-mir-181a-1, rno-mir-214, rno-mir-296, mmu-mir-376b, mmu-mir-370, mmu-mir-433, rno-mir-433, mmu-mir-466a, rno-mir-383, rno-mir-224, mmu-mir-483, rno-mir-483, rno-mir-370, rno-mir-377, mmu-mir-542, rno-mir-542-1, mmu-mir-494, mmu-mir-20b, mmu-mir-503, rno-mir-494, rno-mir-376b, rno-mir-20b, rno-mir-503-1, mmu-mir-1224, mmu-mir-551b, mmu-mir-672, mmu-mir-455, mmu-mir-490, mmu-mir-466b-1, mmu-mir-466b-2, mmu-mir-466b-3, mmu-mir-466c-1, mmu-mir-466e, mmu-mir-466f-1, mmu-mir-466f-2, mmu-mir-466f-3, mmu-mir-466g, mmu-mir-466h, mmu-mir-504, mmu-mir-466d, mmu-mir-872, mmu-mir-877, rno-mir-466b-1, rno-mir-466b-2, rno-mir-466c, rno-mir-872, rno-mir-877, rno-mir-182, rno-mir-455, rno-mir-672, mmu-mir-466l, mmu-mir-466i, mmu-mir-466f-4, mmu-mir-466k, mmu-mir-466j, rno-mir-551b, rno-mir-490, rno-mir-1224, rno-mir-504, mmu-mir-466m, mmu-mir-466o, mmu-mir-466c-2, mmu-mir-466b-4, mmu-mir-466b-5, mmu-mir-466b-6, mmu-mir-466b-7, mmu-mir-466p, mmu-mir-466n, mmu-mir-466b-8, rno-mir-466d, mmu-mir-466q, mmu-mir-21b, mmu-mir-21c, mmu-mir-142b, mmu-mir-466c-3, rno-mir-322-2, rno-mir-503-2, rno-mir-466b-3, rno-mir-466b-4, rno-mir-542-2, rno-mir-542-3
Both ACTH and 17α-E2 up-regulated the expression of miRNA-212, miRNA-132, miRNA-154, miRNA-494, miRNA-872, miRNA-194, and miRNA-24-1, but reduced the expression of miRNA-322, miRNA-20b, miRNA-339, miRNA-27a, miRNA-551b, and miRNA-1224. [score:8]
[1 to 20 of 1 sentences]
18
[+] score: 7
Other miRNAs that approached significance included miR-3553, miR-24-3p, miR-219a-5p, miR-411-5p (upregulated due to stress) and miR-3577 (downregulated due to stress). [score:7]
[1 to 20 of 1 sentences]
19
[+] score: 7
Conversely, stress upregulated miR-24-1. The putative gene targets for these miRNAs were related to neuropathologies, neurotransmission, hormonal regulation, neurotrophic factors, stress response, oxidative stress and metabolism (Figure 2C). [score:7]
[1 to 20 of 1 sentences]
20
[+] score: 6
In contrast, other reports have shown that BIM is downregulated by miR-24 [50], and miR-221 [51], which inhibited apoptosis. [score:6]
[1 to 20 of 1 sentences]
21
[+] score: 6
Additionally, another evidence collected from the current inverstigation demonstrate that the microRNA -mediated regulation is not limited to the 3’UTR, the functionality of target sites in the CDS also confirmed by previous studies [57– 59], such as miR-24 [58], miR-296, miR-470, miR-134 [60], miR-126 [43], miR-181a [59], miR-148 [57] and miR-519 [61] that target sequences within the mRNA coding region have been reported to repress the biosynthesis of the encoded proteins in similar way. [score:6]
[1 to 20 of 1 sentences]
22
[+] score: 6
Six of them, namely, rno-miR-107-5p, rno-miR-383-5p, rno-miR-24-1-5p, rno-mir-191b, rno-miR-196b-5p, and rno-miR-3552, were upregulated, while only rno-mir-194-1 was downregulated in the MCAO group compared with the sham group. [score:6]
[1 to 20 of 1 sentences]
23
[+] score: 5
In the set of depleted miRs, we found miR-24 to control 262 target mRNAs followed by miR-324-3p which controlled 215 targets. [score:5]
[1 to 20 of 1 sentences]
24
[+] 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-23b, 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]
[1 to 20 of 1 sentences]
25
[+] score: 4
Three miRNAs were downregulated: miR-347 (FC = 0.38 ± 0.09; p = 0.019); miR-28-5p (FC = 0.83 ± 0.02; p = 0.005); and miR-24-3p (FC = 0.84 ± 0.02; p = 0.020). [score:4]
[1 to 20 of 1 sentences]
26
[+] score: 4
In addition, compared to F0-N rats, stress in F0-S dams induced one miRNA (rno-miR-466b-1-3p) and suppressed the expression of three miRNAs (rno-miR-145-3p, rno-miR-24-1-5p and rno-miR-375) (all Ps <0.10). [score:4]
[1 to 20 of 1 sentences]
27
[+] score: 4
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-17, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-29a, hsa-mir-30a, hsa-mir-31, hsa-mir-32, hsa-mir-33a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-106a, mmu-let-7g, mmu-let-7i, mmu-mir-27b, mmu-mir-30a, mmu-mir-30b, mmu-mir-126a, mmu-mir-9-2, mmu-mir-135a-1, mmu-mir-137, mmu-mir-140, mmu-mir-150, mmu-mir-155, mmu-mir-24-1, mmu-mir-193a, mmu-mir-194-1, mmu-mir-204, mmu-mir-205, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-143, mmu-mir-30e, hsa-mir-34a, hsa-mir-204, hsa-mir-205, hsa-mir-222, mmu-let-7d, mmu-mir-106a, mmu-mir-106b, hsa-let-7g, hsa-let-7i, hsa-mir-27b, hsa-mir-30b, hsa-mir-135a-1, hsa-mir-135a-2, hsa-mir-137, hsa-mir-140, hsa-mir-143, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-126, hsa-mir-150, hsa-mir-193a, hsa-mir-194-1, mmu-mir-19b-2, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, mmu-mir-200a, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-15a, mmu-mir-23a, mmu-mir-24-2, mmu-mir-29a, mmu-mir-31, mmu-mir-92a-2, mmu-mir-34a, rno-mir-322-1, mmu-mir-322, rno-let-7d, rno-mir-329, mmu-mir-329, rno-mir-140, rno-mir-350-1, mmu-mir-350, hsa-mir-200c, hsa-mir-155, mmu-mir-17, mmu-mir-25, mmu-mir-32, mmu-mir-200c, mmu-mir-33, mmu-mir-222, mmu-mir-135a-2, mmu-mir-19b-1, mmu-mir-92a-1, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-7b, hsa-mir-194-2, mmu-mir-194-2, hsa-mir-106b, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-30e, hsa-mir-375, mmu-mir-375, mmu-mir-133b, hsa-mir-133b, rno-let-7a-1, rno-let-7a-2, rno-let-7b, rno-let-7c-1, rno-let-7c-2, rno-let-7e, rno-let-7f-1, rno-let-7f-2, rno-let-7i, rno-mir-7b, rno-mir-9a-1, rno-mir-9a-3, rno-mir-9a-2, rno-mir-17-1, rno-mir-19b-1, rno-mir-19b-2, rno-mir-23a, rno-mir-24-2, rno-mir-25, rno-mir-27b, rno-mir-29a, 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-32, rno-mir-33, rno-mir-34a, rno-mir-92a-1, rno-mir-92a-2, rno-mir-106b, rno-mir-126a, rno-mir-135a, rno-mir-137, rno-mir-143, rno-mir-150, rno-mir-193a, rno-mir-194-1, rno-mir-194-2, rno-mir-200c, rno-mir-200a, rno-mir-204, rno-mir-205, rno-mir-222, hsa-mir-196b, mmu-mir-196b, rno-mir-196b-1, mmu-mir-410, hsa-mir-329-1, hsa-mir-329-2, mmu-mir-470, hsa-mir-410, hsa-mir-486-1, hsa-mir-499a, rno-mir-133b, mmu-mir-486a, hsa-mir-33b, rno-mir-499, mmu-mir-499, mmu-mir-467d, hsa-mir-891a, hsa-mir-892a, hsa-mir-890, hsa-mir-891b, hsa-mir-888, hsa-mir-892b, rno-mir-17-2, rno-mir-375, rno-mir-410, mmu-mir-486b, rno-mir-31b, rno-mir-9b-3, rno-mir-9b-1, rno-mir-126b, rno-mir-9b-2, hsa-mir-499b, mmu-let-7j, mmu-mir-30f, mmu-let-7k, hsa-mir-486-2, mmu-mir-126b, rno-mir-155, rno-let-7g, rno-mir-15a, rno-mir-196b-2, rno-mir-322-2, rno-mir-350-2, rno-mir-486, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
For instance, among the 66 uniformly expressed miRNAs for which IPA assigned functions, we identified 12 candidates that have been implicated in androgen regulation, including: let-7a-5p, miR-15a-5p, miR-17-5p, miR-19b-3p, miR-23a-3p, miR-24-3p, miR-27b-3p, miR-30a-5p, miR-34a-5p, miR-140-5p, miR-193a-3p, miR-205-5p (S1 Fig). [score:4]
[1 to 20 of 1 sentences]
28
[+] score: 4
Indeed, we have reported decreases in miR-24-3p and miR-34a-5p expression at 5 h post-LTP in awake adult rats (Ryan et al., 2012), and others have shown regulation of specific miRNA both in anaesthetized rats (Wibrand et al., 2010, 2012) and in vitro (Park and Tang, 2009; Lee et al., 2012). [score:4]
[1 to 20 of 1 sentences]
29
[+] score: 3
The values were normalized to miR-24 and are shown in log10 scale on the Y-axis. [score:1]
Hepatic cell and culture medium miR-27a levels were normalized using RNU6 and cel-miR-39 as a reference, whereas serum miR-27a was normalized to miR-24 [13]. [score:1]
The values were normalized to miR-24. [score:1]
[1 to 20 of 3 sentences]
30
[+] score: 3
Huang S. et al., 2008 [65] published that the microRNA cluster miR-23a∼miR-27a∼miR-24 decreases TGF-β induced tumor suppressive activities in human liver cancer cells (HCC). [score:3]
[1 to 20 of 1 sentences]
31
[+] score: 3
There were 8 miRNAs with fold changes in expression greater than 3 [miR-490-5p (FC = 9.44), miR-547-3p (FC = 4.77), miR-24-1-5p (FC = 3.78), miR-200a-5p (FC = 3.55), miR-139-3p (FC = 3.51), miR-139-5p (FC = 3.46), miR-676 (FC = 3.32), and miR-532-3p (FC = 3.07)]. [score:3]
[1 to 20 of 1 sentences]
32
[+] score: 3
8. Qian L, Van Laake LW, Huang Y, Liu S, Wendland MF, Srivastava D. miR-24 inhibits apoptosis and represses Bim in mouse cardiomyocytes. [score:3]
[1 to 20 of 1 sentences]
33
[+] score: 3
Among miRNAs that were present at higher levels in colostrum whey, let-7i, miR-148b-3p, miR-27b, and miR-125b-3p affect the function of antigen-presenting cells, and miR-15b, miR-24, miR-92a, miR-181a, miR-181c, and miR-181d affect T cell development and function [29], [30], [35]. [score:2]
On the other hand, other miRNAs such as, let-7i, miR-143, miR-148b-3p, miR-15b, miR-17-5p, miR-24, miR-27b, miR-92a, miR-106b, miR-125b-5p, miR-181a, miR-181c, miR-181d, miR-200c, miR-375, miR-107, miR-141, and miR-370, were present at higher levels in colostrum whey than in mature milk whey (Fig. 6). [score:1]
[1 to 20 of 2 sentences]
34
[+] score: 2
Others have been linked to the regulation of vascular smooth muscle cells; these include miR-145, let-7d, miR-24, miR-26a, and miR-146 [13]. [score:2]
[1 to 20 of 1 sentences]
35
[+] score: 2
At 24 hours, five miRNAs (rno-miR-214, rno-miR-99a, rno-miR-363*, rno-miR-100 and rno-miR-340–5p) and at 48 hrs 6 miRNAs (rno-miR-34b, rno-miR-500, rno-miR-24-1*, rno-miR-29b, rno-miR-199a-3p, rno-let-7a) showed the most prominent dysregulation (P < 0.001) (Fig.   7B). [score:2]
[1 to 20 of 1 sentences]
36
[+] score: 2
For instance, we have reported that miR-24 synchronously regulates four MODY (Mature Onset of Diabetes of the Young) genes 16. [score:2]
[1 to 20 of 1 sentences]
37
[+] 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]
[1 to 20 of 1 sentences]
38
[+] score: 1
1 up 3.7 down 12 down 1.1 miR-10a up 6.4 up 5.2 up 3.5 down 116 down 1.6 snoRNA202 up 3.8 up 4.7 up 3.2 down 6 down 3 miR-27b down 1.4 up 1.9 up 3.2 up 1 up 1 miR-29c up 5.4 up 4.5 up 3.1 up 1.5 down 1.5 miR-345-5p up 14.3 up 31.7 up 2.4 down 4.7 up 1.1 rno-miR-24-1 down 25.3 up 1.2 up 2.1 down 1.2 down 1.9 miR-687 up 3.8 up 1.8 up 2 down 1.7 down 11.5 miR-27a up 34 up 12. [score:1]
[1 to 20 of 1 sentences]
39
[+] score: 1
Recently, several other miRNAs including miR-24 and miR-182 was implicated to be important for insulin biosynthesis [20]. [score:1]
[1 to 20 of 1 sentences]
40
[+] score: 1
Seeliger et al. profiled miRNAs in bone tissue from patients with osteoporotic fractures and identified five miRNAs, miR-21, miR-23a, miR-24, miR-100, and miR-125b that are highly associated with osteoporotic fractures [13]. [score:1]
[1 to 20 of 1 sentences]
41
[+] score: 1
Furthermore, several miRNAs, such as miR-199a and miR-214 [14], miR-494 [15], miR-499 [16], and miR-24 [17] are known to protect cells from hypoxia- or ischemia -induced damage. [score:1]
[1 to 20 of 1 sentences]