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34 publications mentioning rno-mir-182

Open access articles that are associated with the species Rattus norvegicus and mention the gene name mir-182. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 285
Other miRNAs from this paper: rno-mir-183, rno-mir-200b, rno-mir-381
Both ectopic LRRC4 overexpression, or the restoration of LRRC4 endogenous expression inhibited the expression of BRD7, locked-nucleic-acid (LNA) -mediated miR-182 and -381 silencing specifically targeted the LRRC4 and led to perturbations in the Ras/Raf/ERK/MAPK and PI-3K/AKT signaling pathways and to down-regulation of BRD7, which inhibited glioma growth. [score:16]
Ectopic LRRC4 overexpression in U251 cells (Figure 5D) and 5-Aza-dC -mediated re -expression of LRRC4 in U251, SF126, and SF767 cells (Figure 5E) led to suppression of BRD7 expression, suggesting that miR-182 and miR-381 silencing inhibited BRD7 expression by targeting LRRC4. [score:15]
Thus, it was suggested that LNA -mediated miR-182 and miR-381 silencing down-regulated the expression of BRD7 by restoring LRRC4 expression in gliomas. [score:8]
0084146.g005 Figure 5LNA-anti-miR-182 and -381 induces LRRC4 up-regulation and BRD7 down-regulation. [score:7]
Suppressing endogenous expression of miR-182 and miR-381, respectively, restored the activation of LRRC4 in gliomas, and inhibited glioma cell proliferation in vitro and growth of subcutaneously transplanted tumor in vivo. [score:7]
LNA-anti-miR-182 and -381 induces LRRC4 up-regulation and BRD7 down-regulation. [score:7]
These results suggested that miR-182 and miR-381 silencing modulated the ERK/MAPK and PI-3K/AKT signaling pathways, thereby inhibiting the expression of AP2, SP1, and E2F6 and promoting c-Myc expression. [score:7]
The results showed that transfection of LNA-anti-miR-182 and -381, but not of the LNA-scrambled controls, inhibited the expression of K-Ras, p-c-Raf, pERK, PI-3K, and pAKT, but had no effects on N-Ras, total ERK, and AKT expressions (Figure 6A). [score:7]
miR-182 and miR-381 silencing induced BRD7 down-regulation by targeting LRRC4. [score:6]
ISH and IHC indicated that LNA-anti-miR-381 and/or LNA-anti-miR-182 treatment increased the expression of LRRC4 and reduced the expression of BRD7 (Figures 4B and S4B). [score:5]
ting indicated that LNA -mediated silencing of miR-182 and -381 led to recovery of LRRC4 expression and reduced BRD7 expression (Figure 5B). [score:5]
miR-182 and miR-381 silencing decreased the expression and activity of AP2, SP1, and E2F6, but increased the expression and activity of c-Myc. [score:5]
The inhibitory effect of the combination treatment with miR-182+miR-381 inhibitors was more robust than single treatments (Figures 4A and S4A). [score:5]
0084146.g006 Figure 6LNA-anti-miR-182 and -381 suppressed the promoter activity of BRD7 by down -regulating AP2, SP1, and E2F6, and up -regulating c-Myc. [score:5]
The miRNA target prediction programs TargetScan and PicTar identified miR-182 interaction sites in the 3′-UTR of LRRC4 (Figure 1A). [score:5]
We found that LNA -mediated miR-182 and -381 silencing decreased the expression of BRD7, which was striking in its similarity to the results obtained with LRRC4 overexpression. [score:5]
Mutant, nuclear protein +200×mutant probe + wild biotin-probe; Competitor, nuclear protein +200×competitor cold probe + wild biotin-probe; No extracts, no nuclear protein + wild biotin-probe; Scrambled, nuclear protein of transfected miRNA negative control + wild biotin-probe; LNA-182, nuclear protein of transfected LNA-miR-182 inhibitors + wild biotin-probe; LNA-381, nuclear protein of transfected LNA-miR-381 inhibitors + wild biotin-probe; LRRC4, nuclear protein of transfected LRRC4 gene + wild biotin-probe. [score:5]
First, we examined the effects of different kinase inhibitors (PD98059 for MEK, and LY294002 for PI-3K) on the miR-182- and miR- 381 -induced expression of the transcription factors. [score:5]
To further test the effects of miR-182 and miR-381 on endogenous LRRC4 and BRD7 expressions, we used simple systemic delivery of an unconjugated, PBS-formulated LNA-anti-miR to antagonize expression of endogenous miR-182 and -381 in U251 cells (Figure 5A). [score:5]
In addition, to determine whether the miR-182 and miR-381 silencing -induced effects on the expressions of AP2, SP1, E2F6, and c-Myc were LRRC4 -dependent, we performed LRRC4 overexpression studies. [score:5]
Mutant, nuclear protein+200×mutant probe + wild biotin-probe; Competitor, nuclear protein +200×competitor wild probe + wild biotin-probe; No extracts, no nuclear protein + wild biotin-probe; Mock, nuclear protein+ wild biotin-probe; PD98059, nuclear protein with PD98059 + wild biotin-probe; LY294002, nuclear protein with PD98059 + wild biotin-probe; Scrambled, nuclear protein of transfected miRNA negative control + wild biotin-probe; LNA-182, nuclear protein of transfected LNA-miR-182 inhibitors + wild biotin-probe; LNA-381, nuclear protein of transfected LNA-miR-381 inhibitors + wild biotin-probe; 182M, nuclear protein of transfected miR-182 mimics + wild biotin-probe; 381M, nuclear protein of transfected miR-381 mimics + wild biotin-probe. [score:5]
LNA-anti-miR-182 and -381 suppressed the promoter activity of BRD7 by down -regulating AP2, SP1, and E2F6, and up -regulating c-Myc. [score:5]
When the glioma-related LRRC4 gene was queried by TargetScan and PicTar software, it was identified as a target gene of miR-182 and miR-381. [score:5]
On the basis of our previous research that LRRC4 is a target gene of miR-381, we confirmed LRRC4 is also the target gene of miR-182. [score:5]
We found that the expressions of miR-182, miR-381 or BRD7 proteins were inversely correlated with expression of LRRC4 in glioma tissues and normal brain tissues (Figure 2A). [score:5]
miRNA-182 and miR-381 or BRD7 expression is inversely related to LRRC4 expression in gliomas. [score:5]
The LNA-anti-miR-182 and -381 transfections also increased Rb expression and decreased E2F3 expression (Figure 3B). [score:5]
The study presented herein demonstrated that LNA -mediated miR-182 and miR-381 silencing in gliomas blocked cell cycle progression in the G0/G1 phase by regulating pRb and E2F3 and inhibited cell proliferation in vitro and growth in vivo. [score:4]
Previous studies have demonstrated that LRRC4, a regulator of miR-182 and miR-381, can inhibit glioma tumorigenicity by modulating receptor tyrosine kinase (RTK) signaling pathways, such as the K-Ras/p-c-Raf/ERK/MAPK and PI-3K/AKT signaling pathways [4], [6]. [score:4]
In the current study, LNA -mediated miR-182 and miR-381 silencing was applied and found to restore the expression of LRRC4 in gliomas. [score:3]
miR-182 and miR-381 silencing inhibited glioma tumorigenicity and induced differentiation. [score:3]
LRRC4 is a target gene of miR-182. [score:3]
Moreover, these kinase inhibitor treatments also reversed the miR-182- and miR-38 -induced BRD7 promoter associations of AP2, SP1, E2F6, and c-Myc (Figure 6F). [score:3]
To evaluate the relevance of the endogenous expressions of miR-182, miR-381, BRD7, and LRRC4, we assessed their expressions in human glioma tissues, as well as in normal brain tissues. [score:3]
In this study, we demonstrated that LRRC4 is also a target of miR-182. [score:3]
miR-182 and miR-381 were also determined to be involved in the pathological progression of astrocytoma by targeting LRRC4. [score:3]
Magnetic resonance imaging (MRI) revealed that administration of miR-182 or miR-381 inhibitors was accompanied by significantly reduced growth of the intracranial transplanted tumors. [score:3]
In addition, there was a positive correlation found between expressions of miR-182 or miR-381 and BRD7 in all glioma tissues, and normal brain tissues. [score:3]
In the present study, we demonstrated that LNA -mediated miR-182 and miR-381 silencing can affect the expression and activity of transcription factors that have binding sites in the BRD7 promoter, including AP2, SP1, E2F6, and c-Myc. [score:3]
Similar patterns were observed for ectopic miR-182 expression or LNA -mediated miR-182 silencing (data not shown). [score:3]
Thus, miR-182 and miR-381 may represent useful therapeutic targets for treatment of these tumors. [score:3]
Treatment of U251 cells with LNA-anti-miR-182 or -381 led to differentiation into astrocyte-like cells, as demonstrated by the induced expression of glial fibrillary acidic protein (GFAP). [score:3]
We further found that the expression of miR-182 and miR-381 or BRD7 and LRRC4 were negatively correlated with the pathological progression of gliomas. [score:3]
The results indicated that expression change of miR-182 and miR-381 in normal brain tissue and different grade gliomas (I: 10 cases; II: 22 cases; III: 23 cases; IV: 12 cases) was consistent to that detected by ISH (Figure 2 A-C). [score:3]
Figure S2 qRT-PCR analysis showing miRNA-182 and miR-381 expression in normal brain and WHO grade I, II, III astrocytomas, and grade IV glioblastoma. [score:3]
U251 cells were transfected with either LNA-scrambled, LNA-anti-miR-182 or -381 for 48 h. LRRC4 and BRD7 expression was assessed by. [score:3]
Specifically, we analyzed the expression and/or the activation of some of the proteins involved in the K-Ras/p-c-Raf/ERK/MAPK and PI-3K/AKT signaling pathways in response to miR-182 and miR-381 silencing. [score:3]
As shown in Figure S2, qRT-PCR was used to furhter verify the expression levels of miR-182 and miR-381 in 19 normal brain tissue samples and 67 primary gliomas. [score:3]
0084146.g001 Figure 1 LRRC4 is a target gene of miR-182. [score:3]
Figure S4 (A) Intraperitoneal injection of LNA-anti-miR-182 and/or -381 oligonucleotides surpassed the blood-brain barrier in Sprague-Dawley rats and inhibited the growth of intracranial transplanted tumors. [score:3]
miR-182 and miR-381 expression levels were assessed by ISH. [score:3]
Therefore, we investigated the signal transduction pathways involved in BRD7 expression that was inhibited by miR-182 and -381 silencing. [score:3]
miR-182, miR-381, BRD7 are inversely correlated with LRRC4 expression in gliomas. [score:3]
LRRC4 is a bona fide target of miR-182. [score:3]
0084146.g004 Figure 4 (A) Intraperitoneal injection of LNA-anti-miR-182 and/or -381 oligonucleotides inhibited the growth of intracranial transplanted tumors in Sprague-Dawley rats (top and middle, MRI; bottom, HE staining of coronal section). [score:3]
We confirmed that LRRC4 is a common bona fide target of miR-182 (Figure 1B) by performing luciferase reporter assays. [score:2]
miR-182 and miR-381 silencing regulated AP2/SP1/E2F6/c-Myc -mediated BRD7 transcription induced by LRRC4 -mediated K-Ras/c-Raf/ERK/MAPK and PI-3K/AKT signaling pathways. [score:2]
Our results indicated that, compared with the LNA-anti-scrambled control, transfection of LNA-anti-miR-182 and -381 increased and decreased the expression levels of c-Myc and AP2, SP1, and E2F6 in U251 cells, respectively (Figure 6B). [score:2]
To directly test the functional roles of miR-182 and miR-381 in cell proliferation, ectopic miR-182 and miR-381 mimics or LNA-anti-miR-182 and -381 oligonucleotides were transfected into multiple glioma cell lines. [score:2]
However, compared with treatment with either LNA-anti-miR-182, LNA-anti-miR-381 or 5-Aza-dC alone, the combination treatment of LNA-anti-miR-182/5AZa, LNA-anti-miR-381/5AZa, or LNA-anti-miR-182/LNA-anti-miR-381 did not induce any obvious differences in the growth inhibition of U251 cells (Figure S3). [score:2]
More importantly, we also found that miR-182, miR-381 and BRD7 were inversely correlated with LRRC4 in astrocytomas of various pathological grades (Figure 2B, C), and the extent of correlation increased from WHO grade I to IV. [score:1]
miR-182 or miR-381 mimics and LNA -modified Anti-miR-182 or -381 oligonucleotide transfection. [score:1]
miR-182 or miR-381 miRCURY™ LNA custom detection probes (Exiqon, Vedbaek, Denmark) were used for ISH. [score:1]
The precise roles of miR-182 and miR-381 in relation to LRRC4 expression in gliomas were investigated by the miRNA silencing tool of locked nucleic acids. [score:1]
pMIR-REPORT vectors harboring wild-type (WT) or mutant 3′-UTR LRRC4 sequences were co -transfected into cells along with the miR-182 or miR-381 constructs using Lipofectamine 2000 (Invitrogen, Carlsbad, CA, USA). [score:1]
There were obvious increases in the proliferation of U251, U87, and P19 cells by 24 h after transfection with the miR-182 and -381 mimics. [score:1]
LNA-anti-miR-182 and -381 had anticancer effects on intracranial transplanted tumors by surpassing the blood-brain barrier. [score:1]
The miR-182 mimic (sense: 5′-UUUGGCAAUGGUAGAACUCACACU-3′; anti-sense: 5′-UGUGAGUUCUACCAUUGCUAAAUU-3′), miR-381 mimic (sense: 5′-UAUACAAGGGCAAGCUCUCUGUTT-3′; anti-sense: 5′-ACAGAGAGCUUGCCCUUGUCGCTT-3′), scrambled mimic (sense: 5′-UUCUCCGAACGUGUCACGUTT-3′; anti-sense: 5′-ACGUGACACGUUCGGAGAATT-3′), anti-miR-182 LNA oligonucleotide (5′-LNA-AGUGUGAGUUCUACCAUUGCCAAA-3′), miR-381 LNA oligonucleotide (5′-LNA-ACAGAGAGCUUGCCCUUGUAUA-3′), and scrambled LNA oligonucleotide (5′-LNA-CAGUACUUUUGUGUAGUACAA-3′) were synthesized by GenePharma and were transfected into cells using Lipofectamine 2000. [score:1]
These results indicated that miR-182 and miR-381 silencing interfered with or promoted the binding of various transcription factors to the BRD7 promoter. [score:1]
As evidenced by EMSA, transfections of LNA-anti-miR-182 or -381 disrupted the association of AP2, SP1, and E2F6 with the BRD7 promoter, and promoted association of c-Myc with the BRD7 promoter (Figure 6D). [score:1]
Spearman's correlation test was used to evaluate the pairwise expression correlation between miR-182, miR-381, BRD7 and LRRC4 in gliomas. [score:1]
A cell-cycle analysis showed that transfection of LNA-anti-miR-182 and -381 into U251 cells led to a decrease in the proportion of cells in the S and G2-M phases and a corresponding increase in cells in the G1 phase. [score:1]
Next, we investigated whether the LNA-anti-miR-182 and/or -381 was able to surpass the blood-brain barrier and inhibit growth of the intracranial transplanted tumors. [score:1]
Treatment with PD98059 or LY294002 abrogated the effects induced by the miR-182 and miR-381 mimics (Figure 6C). [score:1]
LNA-anti-miR-182 and -381 had anticancer effects on glioma cells and subcutaneously transplanted tumors in nude mice. [score:1]
It was also found that LNA -mediated miR-182 and miR-381 silencing induced marked differentiation of tumor cells towards a non-cancerous status. [score:1]
The transplanted rats were treated with intraperitoneal injections of 200 µL of 0.9% saline solution containing: 2 µg of scrambled, LNA-anti-miR-182, or LNA-anti-miR-381, or 1 µg of LNA-anti-miR-182+1 µg of LNA-anti-miR-381 over one day. [score:1]
Aliquots of 200 µL of 0.9% saline solution containing 2 µg of scrambled, LNA-anti-miR-182, or LNA-anti-miR-381, or 1 µg of LNA-anti-miR-182+1 µg of LNA-anti-miR-381 were administered via intraperitoneal injection for one day. [score:1]
LNA-anti-miR-182 or LNA-anti-miR-381. [score:1]
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2
[+] score: 165
It has been reported that miR-182 is under the transcriptional regulation of HIFα 39, and inhibition of GSK3β resulted in decreased proteasomal destruction of HIF1α 40, suggesting possible involvement of HIF1α in the compound 5 -induced up-regulation of miR-182. [score:7]
We screened our in-house chemical library, including receptor agonists and antagonists, kinase inhibitors, and ion channel activators and inhibitors, for the ability to increase miR-182 expression in hypoxic cardiomyocytes. [score:7]
Treatment with compound 5 alone or co-treatment with compound 5 and miR-182 (100 nM) completely suppressed BNIP3 expression; however, when high concentrations of anti-miR-182 (100 nM) were co- delivered with compound 5 and miR-182 (100 nM), BNIP3 expression was detectable (Supplementary Fig. 8C). [score:7]
Compound 5 induced miR-182 expression and subsequent BNIP3 down-regulation is independent of β-catenin pathway. [score:6]
Additionally, we examined the effect of increasing concentrations of anti-miR-182 (20, 50, and 100 nM) on the presumably miR-182 -mediated down-regulation of BNIP3 expression in cardiomyocytes under hypoxic conditions. [score:6]
Although we were unable to identify the transcription factor by which compound 5 up-regulates miR-182 expression in cardiomyocytes in the present study, additional transcriptional factors are currently being examined in our laboratory as potential pivotal factors in this process. [score:6]
Treatment with the miR-182 mimic significantly mitigated several hypoxia -induced effects, including the suppression of BNIP3 expression (Fig. 2A), the reduction of pro-apoptotic signaling (Fig. 2B), and the attenuation of mitochondrial fission (Fig. 2C), each of which is typically observed in the setting of BNIP3 -induced apoptosis 23. [score:5]
miR-182 suppresses hypoxia -induced BNIP3 expression and apoptotic events. [score:5]
When either the miR-182 mimic (locally applied to the border zone in gel) or compound 5 (systemically delivered via intravenous injection) was applied immediately following I/R injury, various markers of cell death (necrosis, autophagy, and apoptosis) and the expression of BNIP3 were suppressed in the I/R-injured heart (Supplementary Fig. 11A). [score:5]
Thus, we examined whether compound 5 -mediated increase of miR-182 expression was β-catenin -dependent by using a β-catenin inhibitor (FH535) 38. [score:5]
Among the small molecules screened for their ability to induce miR-182 expression under hypoxic conditions, kenpaullone increased the expression of miR-182 most significantly (Fig. 3A) and did so in a concentration -dependent manner up to 10 μM (Fig. 3B). [score:5]
Among these 8 miRNA candidates, miR-182 most effectively suppressed the hypoxia -induced increase in BNIP3 expression per results of mimic treatment (Supplementary Fig. 3). [score:5]
Furthermore, we observed that the expression levels of BNIP3 and miR-182 under hypoxic conditions were inversely proportional to each other (Fig. 1A), indicating that BNIP3 may be a target for miR-182 in cardiomyocytes. [score:5]
Anti-miR-182 alone did not further increase the expression of BNIP3 in cardiomyocytes under hypoxic conditions (Fig. 1B), suggesting that the expression level of miR-182 may have been too low to be significant. [score:5]
This indicates that 100 nM may be sufficient to abrogate the effects of the delivered exogenous miR-182; it also indirectly shows that the observed down-regulation of BNIP3 with miR-182 was indeed mediated by miR-182. [score:5]
Transfection of miR-182 suppressed the expression of luciferase in cells with the wild type miR-182 binding site, but not in cells with the scrambled miR-182 binding site. [score:5]
These data demonstrate that the down-regulation of BNIP3 via the exogenous delivery of miR-182 mimics effectively prevents the activation of pro-apoptotic processes in cardiomyocytes under hypoxic conditions. [score:4]
Additionally, anti-miR-182 (50 nM) attenuated compound 5 -mediated BNIP3 down-regulation (Supplementary Fig. 8B). [score:4]
Furthermore, compound 5 -mediated down-regulation of BNIP3 under hypoxic conditions was not reversed by FH535 pre-treatment (Supplementary Fig. 9B), indicating that the classical GSK3β/β-catenin pathway is not the major mechanism underlying miR-182 induction. [score:4]
BNIP3 is a direct target of miR-182. [score:4]
Another candidate transcription factor is signal transducer and activator of transcription 5 (STAT5) that has been reported to facilitate interleukin 2 (IL-2) -induced up-regulation of miR-182 in helper T lymphocytes 41. [score:4]
Moreover, the expression of ventricular myosin light chain-2 (MLC-2v), a key regulator of cardiac muscle contraction 42 43, was relatively well-preserved by both miR-182 and compound 5 treatment (Supplementary Fig. 12). [score:4]
Out of 10 compounds (Kenpaullone and 9 derivatives) tested, the compound 5 having a nitro substituent was most effective in inducing miR-182 expression (Supplementary Fig. 7B), and the effect was concentration dependent (Supplementary Fig. 7C). [score:3]
Synthesis of kenpaullone derivatives and their effect on miR-182 and BNIP3 expression. [score:3]
To examine whether changing the substituents of kenpaullone would enhance the ability to induce miR-182 expression, we synthesized 9 derivatives, which were derived from the Fischer indole reactions of 3,4-dihydro-1H-benzo[b]azepine-2,5-dione 11 with various substituted phenylhydrazines under acidic conditions 33 34. [score:3]
These data indicate that miR-182 targets the 3′UTR region of BNIP3 mRNA in a sequence-specific manner (Fig. 1C). [score:3]
Connexin 43 (Cx43) plays an important role in intercellular electrical and metabolic coupling, as well as cytoprotection 44, and the expression of Cx43 was increased by both miR-182 and compound 5 (Supplementary Fig. 13). [score:3]
When 100 nM of anti-miR-182 was co- delivered with miR-182 (100 nM), BNIP3 expression was recovered (Supplementary Fig. 4). [score:3]
miR-182 suppresses hypoxia -induced apoptotic events. [score:3]
Additionally, it has been reported that β-catenin induced miR-182 expression in breast cancer 37. [score:3]
miR-182 inducing small molecule Kenpaullone suppresses hypoxia -induced apoptosis. [score:3]
To further demonstrate that miR-182 targets the 3′UTR region of BNIP3 mRNA, we utilized luciferase reporter constructs containing wild or scrambled miR-182 binding sites of the BNIP3 3′UTR. [score:3]
The expression of BNIP3 and miR-182 were compared at matching time points. [score:2]
Pre-treatment with FH535 failed to prevent the compound 5 -induced increase of miR-182 under hypoxic conditions (Supplementary Fig. 9A). [score:1]
Altogether, these data strongly suggest that the improved survival of cardiomyocytes via miR-182 and compound 5 treatment may have resulted in improved cardiac function following I/R injury. [score:1]
Effect of miR-182 and compound 5 on cardiac cell death in vitro and in vivoTo examine the effect of compound 5 on cardiomyocyte apoptosis in vitro, the cells were exposed to hypoxia with treatment of compound 5, miR-182, anti-miR-182, or their combinations (Supplementary Fig. 10). [score:1]
, Korea) were used a final concentration of 100 and 20 to 100 nM for miRNA-182 and for anti-miRNA-182, respectively. [score:1]
miR-182 expression was measured by real-time PCR. [score:1]
Relative miR-182 expression was measured by real-time PCR. [score:1]
To examine the effect of compound 5 on cardiomyocyte apoptosis in vitro, the cells were exposed to hypoxia with treatment of compound 5, miR-182, anti-miR-182, or their combinations (Supplementary Fig. 10). [score:1]
The immunohistochemical staining of CD31, a well-known endothelial cell marker, demonstrated that miR-182 and compound 5 increased the number of capillaries in the heart. [score:1]
Screening of small molecule inducer of miR-182. [score:1]
For co- delivery of miR-182 and anti-miR-182, miR/lipid and anti-miRNA/lipid complex were prepared separately, but added to culture medium simultaneously. [score:1]
The results of the ongoing investigation on the other transcription factors, including but not limited to, HIF1α and STAT5, will provide more clues on the underlying mechanisms of compound 5 -mediated expression of miR-182 in further studies. [score:1]
These data indicate that the observed decrease of BNIP3 was indeed mediated by (5 -induced) miR-182. [score:1]
Treatment with compound 5 or compound 5 and miR-182 attenuated hypoxia -induced apoptosis of cardiomyocytes, while the addition of anti-miR-182 diminished the anti-apoptotic effect of compound 5 and miR-182. [score:1]
Trichrome staining of the heart demonstrated that both miR-182 and compound 5 significantly attenuated cardiac fibrosis (Fig. 4A). [score:1]
The luciferase activity of the cells only transfected with each vector served as controls for each vector group with relative value of 1. (A) The expression of BNIP3 under hypoxia with or without miR-182 transfection was evaluated by western blot. [score:1]
Effect of miR-182 and compound 5 on cardiac cell death in vitro and in vivo. [score:1]
Together, these data indicate that kenpaullone is a small molecular inducer of miR-182 which exerts anti-apoptotic effects on cardiomyocytes exposed to hypoxia. [score:1]
To further verify the anti-cell death effects of miR-182 and compound 5 in vivo, we utilized a rat heart I/R injury mo del. [score:1]
For mutant pmirGLO vector (pmiR-GLO scrambled Bnip3-3′UTR), scrambled miR-182 binding sequence (GCUAGUA) was used instead of wild miR-182 binding sequence (UUGCCAA). [score:1]
Mature specific miRNA-182 or anti-miRNA-182 and negative control miR (Genolution Pharmaceuticals, Inc. [score:1]
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[+] score: 163
As the miR-182 has downregulated expression that the PTEN can express higher level than usual, the upgoing expressed PTEN will attenuate the signal of insulin that come to the potential insulin resistance. [score:10]
Currently, report has shown that miR-182 is in the positive regulation toward insulin secretion by inhibiting the expression of BHLHE22 which is a molecule that can downregulate insulin mRNA transcription in islet [50]. [score:9]
Therefore, the tissues and organs which detected the differentially expressed miR-182 in the previous studies and the valid target genes of miR-182 were summarized and shown in Table 2. The references which provided the valid target genes of miR-182 were listed in Table S4. [score:7]
In addition, we divided the animal samples into the normal diet and high diet group which can provide general view of the idea that miR-182 is conserved, downregulated, and expressed in any diet conditions. [score:6]
Moreover, the symbol of downregulated expression of miR-182 is consistent whether in the blood sample or the peripheral organ samples. [score:6]
Moreover, the downregulated expression of miR-182 was represented consistently in these tissues as well. [score:6]
In our results, miR-182 is in conserved downregulated expression across the species such as human, rat, and cynomolgus macaque. [score:6]
In this case, the downregulated miR-182 is may possibly become a biomarker in detecting the potential T2D which makes benefits to the medical development. [score:5]
By observing the target genes of miR-182, the gene PTEN is under its suppression [48, 49]. [score:5]
Therefore, it is in high possibility that serious downexpression of miR-182 increases expression of FOXO1 which contributes to hyperglycemia in diabetes [43, 44]. [score:5]
The references and specific expressed tissues of the valid target genes of miR-182. [score:5]
Moreover, the downregulated expression of miR-182 is consistent with the previous study in the blood plasma samples of human and rat [6] and the microarray experiment in peripheral blood with lean and obese human (Accession number: GSE27645; significance was calculated by t-test). [score:4]
Such phenomenon may be explained as the miR-182 was downregulated during T2D and hence causing the insulin mRNA transcripts to decrease. [score:4]
Moreover, as the miR-182 showed close relationship to the T2D syndrome, regulating the expression level of miR-182 might be a possible strategy of treating T2D. [score:4]
The general putative regulation network is summarized in Figure 3. In our study, miR-182 was in the highest copy number among the whole differentially expressed miRNAs. [score:4]
Two genes, BCL2 and BAX, that led to the processes of antiapoptosis and apoptosis are under suppression of miR-182, respectively [52, 53]. [score:3]
By analyzing the target genes of miR-182, the underlying mechanism can be deduced which give us hints to understand about miR-182's functions and relationship to T2D. [score:3]
Therefore, as in the HFD group, in miR-182 expressed lower than that in intact group, the individuals may be in more serious insulin resistance. [score:3]
From the previous studies, it is known that the expression of the gene Foxo1 is under the modulation of the miR-182 [40, 41]. [score:3]
In this study, we used the cynomolgus macaque as T2D animal mo del for doing the miRNA profile analysis for the first time and finally got the same result of differential expressed miR-182 toward the previous experiments done by human and rat. [score:3]
In our study, miR-182 was in the highest copy number among the whole differentially expressed miRNAs. [score:3]
While the individual gets sick in T2D, the balance of the internal environment can get into dysfunction and the miR-182 therefore becomes downexpressed which influences the process of T2D. [score:3]
It can obviously be observed that the miR-182 was in the significant differential expression in the All, intact, and HFD groups, especially in the All compare that reached the entire criteria (P < 0.05 in t-test and ANOVA test, fold change >2). [score:3]
The ANOVA test also proved that, in the expression of miR-182, the interaction between HFD and T2D was not significant (P value = 0.24). [score:3]
In the intact and HFD comparison groups, it is noteworthy that miR-182 represented down -expression consistently (both were almost in 2-fold change). [score:3]
In this case, the serious downexpression of miR-182 (~2-fold in intact group and ~4-fold in HFD group) might finally result in increasing ofmRNA level of FOXO1. [score:3]
According to Table 2, the differentially expressed miR-182 detected in the circulating blood can also be detected in the peripheral organs such as adipose, liver, muscle, and pancreas. [score:3]
While the cholesterol gets higher, the miR-182 and SREBP-2 expression level will tend to be lower. [score:3]
It may be linked to the differential expression of miR-182 which enforces the process of apoptosis, because it can be noticed that the miR-182 may be linked to the two opposite processes of cell proliferation and apoptosis. [score:3]
Moreover, in the T2D individuals, the miR-182 in the HFD group was expressed in much lower level than that in the intact group (Table S3). [score:3]
By the further valid target genes analysis, it is represented that the miR-182 has potentially an important role in the pathogenic process of T2D including the insulin resistance, insulin secretion, and the cell apoptosis which potentially cause tissue impairment. [score:3]
In another word, the expression of miR-182 was generally stable in both groups. [score:3]
Interestingly, by comparing the intact-normal and HFD-normal individuals, we found that miR-182 was not in significant expression (Figure 2). [score:3]
In addition, some of the genes such as MYC which is important in the cell cycle regulation [48, 49] and RELA which is in the functions of inflammatory reaction and antiapoptosis are also regulated by miR-182 [54]. [score:3]
Thus, the fate of the cell can be determined by the miR-182 but the underlying mechanism about how to regulate which functions it would perform is still unknown. [score:2]
The relationship of the miR-182 and the mechanism linked to T2D was summarized in Figure 3. From the previous studies, we supposed that the miR-182 can influence the process of T2D to modulate the insulin secretion, attenuate the effect of insulin signaling pathway, and do the possible regulation of the cell's fate. [score:2]
Therefore, further studies to clarify the functions of the miR-182 might be needed for the medical purpose in diagnosis of T2D and therapy development toward T2D. [score:2]
Thus, some important miRNAs including miR-182 can be kept stable so that they cannot get into the endocrinal dysfunction and therefore protect the internal environmental balance. [score:1]
The Syndrome Which Occurs during the T2D Can Be Potentially Linked to the miR-182. [score:1]
In the general view, miR-182 represents a crucial component in the modulation of the molecules during T2D. [score:1]
The miR-182 Can Be a Reliable Biomarker for Diagnosis of T2D. [score:1]
However, in the recent years, little attention was paid to the relationship between miR-182 and T2D. [score:1]
However, currently few reports were focus on the relationship between miR-182 and T2D. [score:1]
Among the 24 specific miRNAs, 13 of them, such as miR-182/196a/381/499a/99a [6], miR-183 [6, 23], miR-409 [23], miR-146b [6, 24], miR-143 [6, 24], miR-148a [24, 25], miR-204 [5], and miR-9 [6], have been reported to involve in T2D process in mouse or rat. [score:1]
Therefore, it cannot simply be said that the level of miR-182 is only related to the cholesterol level. [score:1]
3.4. miR-182 as a Crucial miRNA in the T2D Individuals. [score:1]
Therefore, it can be obviously noticed that miR-182 is closely related to T2D and might influence or lead to some of the syndromes during T2D. [score:1]
Four microRNAs, including miR-9, miR-1285-3p, miR-424-3p, and miR-182-5p, were filtered in all three comparisons. [score:1]
Therefore, because of the characteristics of miR-182 that keeps stable in the healthy individuals but downexpressed in the T2D period no matter in the lean or obese individuals, it comes to be a reliable biomarker for diagnosis of T2D. [score:1]
Thus, such case may contribute to the greater fold change of miR-182 in HFD group than intact group (Figure 1). [score:1]
Thus, miR-182 might be in close relationship to T2D. [score:1]
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4
[+] score: 115
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-24-1, 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-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
The expression levels of miR-183, miR-96, and miR-182 were most highly up-regulated, whereas miR-122, miR-503, and miR-139-3p exhibited the greatest down-regulation as a result of 17α-E2 treatment. [score:9]
The expression levels of miR-183 (4.61-fold), miR-96 (4.56-fold), and miR-182 (4.29-fold) were most highly up-regulated, whereas miR-122 (9.79-fold), miR-503 (5.88-fold), and miR-139-3p (1.94-fold) showed the greatest down-regulation as a result of 17α-E2 treatment. [score:9]
ACTH up-regulated the expression of miRNA-212, miRNA-182, miRNA-183, miRNA-132, and miRNA-96 and down-regulated the levels of miRNA-466b, miRNA-214, miRNA-503, and miRNA-27a. [score:9]
Real-time PCR (qRT-PCR) measurements demonstrated that ACTH treatment upregulated the expression of miRNA-212, miRNA-183, miRNA-182, miRNA-132 and miRNA-96, while down -regulating the expression of miRNA-466b, miRNA-214, miRNA-503 and miRNA-27a. [score:7]
Treatment of MLTC-1 cells with Bt [2]cAMP for 6 h increased the expression of miRNA-212, miRNA-183, miRNA-132, miRNA-182 and miRNA-96 and inhibited the expression of miRNA-138 and miRNA-19a (Fig. 4B ). [score:7]
The levels of miR-212, miRNA-183, miRNA-182, miRNA-132, miRNA-370, miRNA-377, and miRNA-96 were up-regulated, whereas miR-125b, miRNA-200b, miR-122, miRNA-466b, miR-138, miRNA-214, miRNA-503 and miRNA27a were down-regulated in response to 17α-E2 treatment. [score:7]
qRT-PCR measurements confirmed that the expression of miR-212, miRNA-183, miRNA-182, miRNA-132, miRNA-370, miRNA-377 and miRNA-96 was up-regulated and that of miRNA-122, miRNA-200b, miRNA-466b, miRNA-138, miRNA-214, miRNA-503 and miRNA-27a down-regulated in adrenals from 17α-E2 treated rats (Fig. 3 ). [score:7]
Real-time quantitative PCR measurements confirmed that the expression of miR-212, miRNA-183, miRNA-182, miRNA-132, miRNA-370, miRNA-377 and miRNA-96 was up-regulated and that of miRNA-122, miRNA-200b, miRNA-466b, miRNA-138, miRNA-214, miRNA-503 and miRNA-27a down-regulated in adrenals from 17α-E2 treated rats. [score:7]
Treatment of MLTC-1 cells with Bt [2]cAMP for 6 h increased the expression of miRNA-212, miRNA-183, miRNA-132, miRNA-182 and miRNA-96, and inhibited the expression of miRNA-138 and miRNA-19a. [score:7]
Bt [2]cAMP stimulation of granulosa cells caused down-regulation of a majority of miRNAs, including miRNA-200b, miRNA-466b, miRNA-27a, miRNA-214, miRNA-138 and miRNA-19a, but expression levels of miRNA-212, miRNA-183, miRNA-182, and miRNA-132 were significantly increased. [score:6]
qRT-PCR measurements indicated that exposure of primary rat granulosa cells to Bt [2]cAMP for 24 h inhibited the expression of miRNA-200b, miRNA-466b, miRNA-27a, miRNA-214, and miRNA-138 and miRNA-19a while enhancing the expression of miRNA-212, miRNA-183, miRNA-182, and miRNA-132 (Fig. 4 ). [score:5]
NR5A1 was predicted to be the target gene of miR-342, while LDL-R was predicted to be the target gene of miR-182 and miR-466b. [score:5]
Here, we directly assessed the binding of miRNA-138, miRNA-132 and miRNA-182/miRNA-214 to the 3′UTR of StAR, SREBP-1c, and LDLR, respectively, and regulation of their expression levels, by carrying out luciferase reporter gene assays. [score:4]
Real-time PCR (qRT-PCR) confirmed ACTH -mediated up-regulation of miRNA-212, miRNA-183, miRNA-182, miRNA-132 and miRNA-96. [score:4]
Microarray data demonstrated that the levels of miR-183 and miR-182 were up-regulated with 17α-E2 treatment, but not with ACTH (p = 0.065) treatment; qRT-PCR measurements, however, showed significant increases in their expression in response to either ACTH or 17α-E2 treatment. [score:4]
In contrast, no inhibitory effect of pre-miRNA-138 on the StAR 3′ UTR (with 2 putative binding sites) reporter construct and pre-miRNA-182 on the LDLR 3′UTR (with a single putative binding site) reporter construct was detected. [score:3]
We next evaluated the effects of Bt [2]cAMP stimulation of rat ovarian granulosa cells and of mouse MLTC-1 Leydig tumor cells on the expression of twelve miRNAs (miRNA-212, miRNA-122, miRNA-183, miRNA-200b, miRNA-466b, miRNA-182, miRNA-96, miRNA-27a, miRNA-132, miRNA-214, miRNA-138 and miRNA-19a) whose adrenal expression was differentially altered in response to treatment of rats with ACTH, 17α-E2 or DEX. [score:3]
The levels of expression of miRNA-212, miRNA-122, miRNA-138, miRNA-214, miRNA-183, miRNA-182, miRNA-132, miRNA-96, miRNA-466b, miRNA-200b, and miRNA-19a are shown. [score:3]
More specifically, we assessed the impact of Bt [2]cAMP treatment on the expression of miRNA-212, miRNA-122, miRNA-27a, miRNA-466b, miRNA-200b, miRNA-138, miRNA-214, miRNA-183, miRNA-182, miRNA-132, miRNA-96 and miRNA-19a. [score:3]
CHO cells were co -transfected individually with StAR 3′-UTR (containing the putative site I or site II for miRNA-138 binding) ± pre-miRNA-138-5p (panel B), SREBP-1c 3′-UTR (containing the putative binding site for miRNA-132) ± pre-miRNA-132-3p, LDLR 3′-UTR (containing the putative binding site for miRNA-182), or LDLR 3′-UTR (containing the putative site I, site II or site III for miRNA-214 binding) ± pre-miRNA-214-3p for 36h, followed by determination of luciferase activities. [score:1]
Seed sequences of the putative miRNA-138-5p, miRNA-132-3p and miRNA-182-5p/miRNA-214-3p binding sites in the 3′-UTR of mouse StAR, SREBP-1c and LDLR genes, respectively. [score:1]
Individual fragments of the 3′ UTR region of the StAR gene containing site I or site II binding site for miRNA-138-5p, the 3′-UTR of SREBP-1c containing a binding site for miRNA-132-5p, the 3′-UTR of LDLR containing a binding site for miRNA-182-5p or the 3′-UTR of LDLR containing site I, site II, or site III binding site for miRNA-214-3p were inserted downstream of the luciferase open reading frame of pMIR-REPORT vector. [score:1]
CHO cells were co -transfected individually with the StAR 3′-UTR (containing putative site I or site II for miRNA-138 binding) ± pre-miRNA-138-5p (panel B), the SREBP-1c 3′-UTR (containing putative binding site for miRNA-132) ± pre-miRNA-132-3p (panel C), the LDLR 3′-UTR (containing putative binding site for miRNA-182) (panel D), or the LDLR 3′-UTR (containing putative site I, site II or site III for miRNA-214 binding) ± pre-miRNA-214-3p for 36 h (panel E). [score:1]
Quantitative RT-PCR (qRT-PCR) validation of miRNA-212, miRNA-200b, miRNA-183, miRNA-122, miRNA-19a, miRNA-466b, miRNA-182, miRNA-132, miRNA-138, miRNA-370, miRNA-96, miRNA-503, miRNA-27a and miRNA-214 levels in control, ACTH-, 17α-E2 or DEX -treated adrenals in vivo. [score:1]
0078040.g003 Figure 3Quantitative RT-PCR (qRT-PCR) validation of miRNA-212, miRNA-200b, miRNA-183, miRNA-122, miRNA-19a, miRNA-466b, miRNA-182, miRNA-132, miRNA-138, miRNA-370, miRNA-96, miRNA-503, miRNA-27a and miRNA-214 levels in control, ACTH-, 17α-E2 or DEX -treated adrenals in vivo. [score:1]
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[+] score: 60
A genetic association study in humans also revealed that subjects with the downregulated miR-182 genotype are more susceptible to Behçet's disease and Vogt-Koyanagi-Harada disease [54]. [score:8]
Importantly, miR-182 was noted to be overexpressed in gliomas and directly suppressed cylindromatosis (CYLD), an NF- κB -negative regulator [52]. [score:7]
In situ hybridization in the iris/ciliary body tissue over the 14 days following disease induction (Figure 4) confirmed the reduced expression of miR-146a-5p and enhanced expression of miR-182-5p in the eyes examined. [score:7]
miR-146a-5p, miR-155-5p, miR-147b, and miR-223-3p were downregulated, while miR-182-5p, miR-183-5p, and miR-9-3p were upregulated. [score:7]
In murine EAU or human sympathetic ophthalmia eyes, miR-182 and miR-183 were downregulated following disease induction and were speculated to be associated with retinal tissue injury [27] and Forkhead box O1 or Fas/Fas ligand system activation [26, 53]. [score:6]
Among the miRNAs studied, miR-146a-5p, miR-155-5p, miR-182-5p, and miR-183-5p are four particularly crucial miRNAs for the following reasons: they all show significant differential profiles in the disease course; they all regulate NF- κB pathway, and miR-146a-5p and miR-155-5p are regarded as potent immunological drivers; they all have been reported in some uveitis mo dels. [score:4]
The expression profile of the miR-182 family in panuveitis has been studied. [score:3]
The complete dynamic profiles of the levels of each miRNA are summarized in Table 1 and Figure 2. Generally, the expression of miR-9-3p, miR-182-5p, and miR-183-5p tended to increase from day 7 after immunization onwards and peaked at day 10 after immunization. [score:3]
The expression levels of miR-146a-5p, miR-155-5p, miR-182-5p, and miR-183-5p in iris/ciliary bodies and popliteal lymph nodes are shown in Figure 3. The levels of miR-146a-5p and miR-155-5p in the popliteal lymph nodes reached their lowest point earlier, on day 7, while those in the iris/ciliary body tissue kept decreasing until day 15 after immunization. [score:3]
We believe that, in the absence of retinal destruction, the cause of miR-182 family overexpression in EAAU is highly likely due to active involvement of NF- κB activation and T cell recruitment. [score:3]
No significant difference was noted in terms of miR-182-5p and miR-183-5p in the popliteal lymph nodes over the course of the disease. [score:3]
Previous evidence has suggested the important role of miR-182 in T cell clonal expansion after the stimulation of T helper cells by IL-2 [50] and regulation of specialization of Treg cells [51]. [score:2]
Blockage of miR-182 led to the improvement of arthritis in an ovalbumin -induced arthritis mouse mo del [50]. [score:1]
Oligonucleotide probes specific for the two selected miRNAs (miR-146a-5p and miR-182-5p) were labeled at the 5′ end with digoxigenin. [score:1]
MiR-182 and miR-183 belong to the same family, and unlike other miRNAs, miR-182 is one of the few dominant miRNAs that can increase more than 100-fold [48]. [score:1]
The eight miRNAs studied were miR-155b-5p, miR-21-5p, miR-146a-5p, miR-9-3p, miR-147b, miRNA-183-5p, miRNA-182-5p, and mi -RNA-223-3p. [score:1]
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6
[+] score: 47
miR-29a, miR-144, miR-150, miR-192 and miR-320 showed an up-regulation from that of control samples whereas miR-30d, miR-146a and miR-182 showed down-regulation. [score:7]
We found miR-182, a potential modulator of FOXO1 to be down-regulated in T2D but was slightly up-regulated in IFG (Fig. 5B, 6A). [score:7]
miR-182 was also down-regulated in all five tissues with the lowest expression observed in skeletal muscle 10.1371/journal. [score:6]
miR-150, miR-182 and miR-30d showed contrasting expressions in IFG and T2D while miR-146a was down-regulated in both cases. [score:6]
Marginal expression levels were observed for miR-182 (−1.267±0.26) and miR-29a (1.351±0.23) which inversely correlated to their respective predicted mRNA targets FOXO1 and AKT2 respectively. [score:5]
miR-144, miR-146, miR-182 and miR-192 showed a lower expression compared to the other miRNAs in the three insulin target tissues as well as in the pancreas. [score:4]
Among the novel miRNAs (miR-144, miR-146a, miR-150 and miR-182) identified, miR-144 had the highest up-regulation upon T2D in most tissues. [score:4]
We identified miR-146a, miR-182 and miR-30d to be among the highly down-regulated miRNAs across all five sources. [score:4]
We have also identified eight important miRNAs (miR-144, miR-146a, miR-150, miR-182, miR-192, mir-29a, miR-30d and miR-320) that could participate in the regulation of insulin signaling as well as useful in distinguishing different stages of diabetes progression. [score:2]
Employing miRNA microarray and stem-loop real-time RT-PCR, we identify four novel miRNAs, miR-144, miR-146a, miR-150 and miR-182 in addition to four previously reported diabetes-related miRNAs, miR-192, miR-29a, miR-30d and miR-320a, as potential signature miRNAs that distinguished IFG and T2D. [score:1]
Predictions: miR-144/ IRS1; miR-146a/ PTPN1; miR-150/ GLUT4 and CBL; miR-182/ FOXO1; miR-192/ INSR; miR-30d/ INS; miR-29a and miR-320/ AKT2. [score:1]
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[+] score: 40
For example, miR-182 targets actin -regulating proteins and its upregulation was linked to disrupted amygdala -dependent fear memory 67. [score:7]
Moreover, miR-182 has been shown to regulate BDNF expression 69, thus proposing a key mechanism for stress to interact with the expression of affective behaviours. [score:6]
Importantly, miR-182 overexpression was found to be associated with depression-like behaviours and decreased hippocampal BDNF expression in stressed rats, and miR-182 silencing led to anti-depressant-like effects 68. [score:5]
Fold changes of the miRNAs of interest differentially expressed in the animals housed in the enriched environment compared to standard housing controls are summarized in Fig. 5. Target prediction and hypergeometric test found pertinent biochemical pathways for miR-182 including neurotrophin signaling (Figure S1) and axon guidance (Figure S2). [score:4]
These data show that miR-182 may regulate BDNF and neurotrophin-3 (NT-3) expression and may be involved in axonal guidance mechanisms particularly involving netrin, semaphorin, and ephrin (Figures S1 and S2). [score:4]
Further studies have also associated miR-182 with the regulation of NT-3 expression. [score:4]
Indeed, miRNAs that were differentially expressed in stress are recognized biomarkers of mental health, including miR-10a-5p in depression 65, miR-219a-5p in schizophrenia 66 and miR-182 in fear memory, depression and synaptic plasticity 67. [score:3]
After adjusting p-values using the Benjamini and Hochberg correction 27, three miRNAs were differently expressed which included miR-182, miR-10a-5p and miR-124-3p (FDR p < 0.05). [score:3]
The present data on miR-182 suggest that an underpinning mechanism is the regulation of axonal pathfinding and synaptic maintenance during development and maturation. [score:3]
Recent findings have highlighted a central role of miR-182 in structural plasticity. [score:1]
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[+] score: 35
The final stable reporter cell line was designed to identify small compounds (e. g. HDAC inhibitor Panobinostat) that inhibit miR-182 (and/or miR-183) generation or function, thereby resulting in the activation of the luciferases (both firefly and Renilla). [score:5]
We used a miR-182 (or miR-183) inhibitor (miRIDIAN microRNA hairpin inhibitor, Thermo Fisher Scientific) as a positive control and non-specific miRNA (miRIDIAN microRNA Negative Control, Thermo Fisher Scientific) as a negative control. [score:5]
[12] We showed that the inhibition of the miR-200 family and/or miR-182 family in SHSY5Y cells increased global protein conjugation by the abovementioned ULMs, and in so doing made these cells more resistant to OGD -induced cell death. [score:3]
As shown in Supplementary Figure 2(c), the basal level of luciferase activities (both firefly and Renilla) are very low in comparison to negative controls in Supplementary Figure 2(a) and (b) and the activation by the miR-182 (or miR-183) inhibitors were substantial. [score:3]
In order to maintain minimal basal levels of luciferase activities, we transduced these stable cell lines with lentiviral particles containing miR-182 (or miR-183) shMIMIC microRNAs (Thermo Fisher Scientific), and in so doing established cell lines that constitutively expressed these miRNAs via the selective pressure of puromycin. [score:3]
Herein we describe the development of a novel qHTS assay designed to uncover small molecules that increase global SUMOylation via inhibition of the miR-182 family. [score:3]
We then examined whether these stable transfectants (miR-182 or miR-183 target sequence in pmirGLO/psiCHECK1 plus lentiviral particles containing miR-182 or miR-183 shMIMIC) were usable for high-throughput screens. [score:3]
The final stable reporter cell line was designed to identify small compounds that inhibit miR-182 (and/or miR-183) generation or function, thereby resulting in the activation of the luciferases (both firefly and Renilla). [score:3]
Starting from these two vectors, we built a dual reporter construct with the miR-182 (or miR-183) target sequence (Figure 1 and Supplementary Figure 1), so that the presence of mature miR-182 or miR-183 would lead to a decrease in luciferase (both firefly and Renilla) signal, enabling the detection of putative miR-182 (or miR-183) levels. [score:3]
Of note, the endogenous levels of both miR-182 and miR-183 are quite low in SHSY5Y cells and thus the basal levels of luciferase activities are quite high (Supplementary Figure 2a and b). [score:1]
As shown in Supplementary Figure 2a, increased miR-182 (or -183) levels induced via the transfection of mimics significantly depressed both firefly and Renilla luciferase activity. [score:1]
The established stable transfectants responded well to both miR-182 or miR-183 mimics (i. e. the transfection of these mimics caused the depression of both firefly and Renilla luciferase acitivities in each cell line (Supplementary Figure 2b)). [score:1]
We confirmed that the presence of mature miR-182 or miR-183 would lead to a decrease in luciferase (both firefly and Renilla) signal, enabling the detection of putative miR-182 (or miR-183) levels (Supplementary Figure 2). [score:1]
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[+] score: 27
Total RNA extracted from Dex/OSM treated AR42J-B13 cells (7 Days) and mock controls were used for Northern blot analysis using antisense probes against down-regulated miRNAs (miR-93, miR-106b and miR-130b) and up-regulated miRNAs (miR-21, miR-22, miR-122a and miR-182). [score:7]
Both up-regulated miRNAs (miR-21, miR-22, miR-122a and miR-182) and down-regulated miRNAs (miR-17-5p, miR-18a, miR-93, miR-106a, miR-106b, miR-130b and miR-375) were chosen as a parameter for comparison. [score:7]
Using these hepatocyte and non-hepatocyte cell lines and primary tissues, we performed unsupervised clustering analysis by selecting 7 down-regulated miRNAs (miR-17-5p, miR-18a, miR-93, miR-106a, miR-106b, miR-130b and miR-375) and 4 up-regulated miRNAs (miR-21, miR-22, miR-122a and miR-182). [score:7]
Mature miRNA of miR-93, miR-106b, miR-130b, miR-21, miR-22 and miR-182 were differentially expressed after transdifferentiation. [score:3]
As shown in Table 2, we found increased expression of liver specific miRNAs in transdifferentiated hepatocytes, including miR-122a, miR-21, miR-22, miR-182, miR-29 and miR-30. [score:3]
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[+] score: 20
At the same time, up-regulation of hsa-miR-181c and hsa-miR-182 targets HRB and IGF1R expression, suggesting the biological functions of the two key genes may be suppressed. [score:10]
To generate a miR-340 expression vector, a ≍260-bp genomic fragment up and downstream of the pre-mir-182 form was amplified by PCR and the fragment containing strictly the pre-miR-340 form was cloned into pGIPZ (Open Biosystems, Pittsburgh, PA, USA) that allows regulated expression of miR-340 upon zeocin treatment. [score:6]
In contrast, the miRNAs hsa-miR-340 (14 degrees), hsa-miR-181c (11 degrees) and hsa-miR-182 (10 degrees) were significantly up-regulated in the DCM samples. [score:4]
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[+] score: 12
Stress also downregulated miRNAs that possess potential roles in the pathogenesis of psychiatric diseases, such as miR-96 [51], miR-182 and miR-183 [52]. [score:6]
The qRT-PCR confirmed changes of the selected miRNAs (Figure  4B), decreased expression of miR-96, miR-141, miR-182, miR-183, miR-200a, miR-200b, miR-429 and miR-451 in F2-SSS compared to F0-S animals, whereas miR-23b and miR-200c showed increased expression levels. [score:4]
In order to validate miRNAs, we performed quantitative real time PCR (qRT-PCR) analysis of these differentially regulated miRNAs (n = 3 per group for F0, F1 and F2 generations, three replicates per sample): miR-23b, miR-96, miR-141, miR-181a, miR-182, miR-183, miR-200a, miR-200b, miR-200c, miR429 and miR-451. [score:2]
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[+] score: 12
miR-182 induces cervical cancer cell apoptosis through inhibiting the expression of DNMT3a. [score:5]
MicroRNA-182 aggravates cerebral ischemia injury by targeting inhibitory member of the ASPP family (iASPP). [score:4]
A recent study reported that iASPP expression was decreased in cerebral ischemia and was modulated by miR-182 [35], an apoptosis inducer [36], which was similar to our previous study [17] and the present study. [score:3]
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13
[+] 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-16-1, hsa-mir-17, hsa-mir-21, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-30a, hsa-mir-31, hsa-mir-96, hsa-mir-99a, hsa-mir-16-2, hsa-mir-30c-2, hsa-mir-30d, hsa-mir-182, hsa-mir-183, hsa-mir-211, hsa-mir-217, hsa-mir-218-1, hsa-mir-218-2, hsa-mir-221, hsa-mir-222, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-23b, hsa-mir-30b, hsa-mir-125b-1, hsa-mir-132, hsa-mir-143, hsa-mir-145, hsa-mir-191, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-184, hsa-mir-190a, hsa-mir-195, rno-mir-322-1, rno-let-7d, rno-mir-335, rno-mir-342, rno-mir-135b, hsa-mir-30c-1, hsa-mir-299, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-379, hsa-mir-382, hsa-mir-342, hsa-mir-135b, hsa-mir-335, rno-let-7a-1, rno-let-7a-2, rno-let-7b, rno-let-7c-1, rno-let-7c-2, rno-let-7e, rno-let-7f-1, rno-let-7f-2, rno-let-7i, rno-mir-15b, rno-mir-16, rno-mir-17-1, rno-mir-21, rno-mir-23a, rno-mir-23b, rno-mir-24-1, rno-mir-24-2, rno-mir-25, rno-mir-26a, rno-mir-26b, rno-mir-30c-1, rno-mir-30e, rno-mir-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-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
MiRNAs found to be primarily down-regulated in DHT -treated rats includes rno-miR-770, rno-miR-466c, rno-miR-21, rno-miR-31, rno-miR-182, rno-miR-183, rno-miR-96, rno-miR-132, rno-miR-182, rno-miR-384-3p and rno-miR-184. [score:4]
Thus, it is possible that the down-regulation of miRNAs (rno-miR-770, rno-miR-466c, rno-miR-31, rno-miR-183, rno-miR-96, rno-miR-132, rno-miR-182, rno-miR-384-3p and rno-miR-184) observed in this study could be associated with promoted thecal hyperandrogenesis [37, 38]. [score:4]
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]
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14
[+] score: 10
Other miRNAs from this paper: rno-mir-27b, rno-mir-27a
Corroborative results were obtained, showing that miR-27a was significantly down-regulated while miR-182 was obviously up-regulated in the Mo del group (Fig. 1c,d). [score:7]
qRT-PCR was performed to determine the expression levels of miR-27a and miR-182, and to verify the microarray analysis. [score:3]
[1 to 20 of 2 sentences]
15
[+] score: 9
Of the 46 increased miRNA, sICAM-1 was the predicted target of 6 (miR-23b, miR-27a, miR-99a, miR-100, miR-324-5p, miR-363); PAI-1 was the predicted target of 4 (miR-30a, miR-30d, miR-182, miR-384-5p), E selectin the predicted target of 2 (miR-16; miR-195) and the alpha chain of fibrinogen the predicted target of miR-29c [26]. [score:9]
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16
[+] score: 9
In addition, treatment of inflammatory cytokines to periodontal ligament cells results in expressional changes of various miRNAs, such as miR-138, miR182 18, 19, suggesting that miRNAs which regulate periodontal tissue development and repair may be affected by inflammatory environmental cytokines and could result in impaired periodontal tissue regeneration. [score:5]
Wang L Long noncoding RNA related to periodontitis interacts with miR-182 to upregulate osteogenic differentiation in periodontal mesenchymal stem cells of periodontitis patientsCell Death Dis. [score:4]
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17
[+] score: 8
Future studies may aim to manipulate the expression of miRNAs such as miR-182 in order to normalize the amygdala -dependent memory impairments in these mice. [score:3]
We demonstrated the presence of miRNAs that had a large fold increase (miR-3535, miR-673-5p) or decrease (miR-182-5p, miR-1964, miR-206-3p), that were normalized by colonization (miR-219a-2-3p (PFC), miR-182-5p, miR-183-5p (amygdala)) and that are known to be implicated in influencing anxiety levels and expression of neurotrophins such as brain-derived neurotrophic factor (BDNF) (miR-183-5p, miR-206-3p) [33, 34]. [score:3]
Within the amygdala, we found that miR-183-5p and miR-182-5p were both decreased and subsequently normalized by colonization. [score:1]
Within the lateral amygdala, miR-182 appears to be essential for long-term amygdala -dependent memory formation assessed by auditory fear conditioning [23]. [score:1]
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18
[+] score: 7
In order, the miRNAs potentially contributing to downregulation of gremlin1 expression were identified as miR-27a/b, miR-23a/b, miR-181a/b/c/d and miR-182 (Figure 4A, 4B). [score:6]
Conserved binding sites for miR-23a/b, miR-27a/b and miR-181a/b/c/d were predicted in 3107–3442 nt region (G3-23-1) and for miR-182 in the 3590–3809 nt region (G3-23-3). [score:1]
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19
[+] score: 6
Dolganiuc et al (13) demonstrated that the Lieber-deCarli alcohol diet upregulated 1% of known miRNAS, including miR-705 and miR-1224, and downregulated 1% of known miRNAs, including miR-182, miR-183 and miR-199a-3p in mice with alcoholic steatohepatitis compared with pair-fed controls. [score:6]
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20
[+] score: 5
In order to validate the changes in miRNA expression detected by a deep-sequencing, we conducted quantitative real-time PCR analysis to examine expression levels of six miRNAs including rno-miR-378, rno-miR-182, rno-miR-21, rno-miR-34a, rno-miR-34b, and rno-miR34c. [score:5]
[1 to 20 of 1 sentences]
21
[+] score: 4
Molecular basis of differential target regulation by miR-96 and miR-182: the Glypican-3 as a mo del. [score:4]
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22
[+] score: 4
MiR-132 was upregulated in SNI rats (Leinders et al., 2016), while miR-182, miR-183, miR-96 decreased in SNL rats (Aldrich et al., 2009). [score:4]
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23
[+] score: 3
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-26b, hsa-mir-29a, hsa-mir-30a, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-106a, mmu-let-7g, mmu-let-7i, mmu-mir-15b, mmu-mir-29b-1, mmu-mir-30a, mmu-mir-30b, mmu-mir-125a, mmu-mir-125b-2, mmu-mir-130a, mmu-mir-138-2, mmu-mir-181a-2, mmu-mir-182, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-30e, hsa-mir-10a, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-182, hsa-mir-181a-1, mmu-mir-297a-1, mmu-mir-297a-2, mmu-mir-301a, mmu-mir-34c, mmu-mir-34b, mmu-let-7d, mmu-mir-106a, mmu-mir-106b, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-30b, hsa-mir-125b-1, hsa-mir-130a, hsa-mir-138-2, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-138-1, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-15a, mmu-mir-26b, mmu-mir-29a, mmu-mir-29c, mmu-mir-34a, rno-mir-301a, rno-let-7d, rno-mir-344a-1, mmu-mir-344-1, rno-mir-346, mmu-mir-346, rno-mir-352, hsa-mir-181b-2, mmu-mir-10a, mmu-mir-181a-1, mmu-mir-29b-2, mmu-mir-138-1, mmu-mir-181b-1, mmu-mir-181c, mmu-mir-125b-1, hsa-mir-106b, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-34b, hsa-mir-34c, hsa-mir-301a, hsa-mir-30e, hsa-mir-362, mmu-mir-362, hsa-mir-369, hsa-mir-374a, mmu-mir-181b-2, hsa-mir-346, rno-let-7a-1, rno-let-7a-2, rno-let-7b, rno-let-7c-1, rno-let-7c-2, rno-let-7e, rno-let-7f-1, rno-let-7f-2, rno-let-7i, rno-mir-10a, rno-mir-15b, rno-mir-26b, rno-mir-29b-2, rno-mir-29a, rno-mir-29b-1, rno-mir-29c-1, rno-mir-30c-1, rno-mir-30e, rno-mir-30b, rno-mir-30d, rno-mir-30a, rno-mir-30c-2, rno-mir-34b, rno-mir-34c, rno-mir-34a, rno-mir-106b, rno-mir-125a, rno-mir-125b-1, rno-mir-125b-2, rno-mir-130a, rno-mir-138-2, rno-mir-138-1, rno-mir-181c, rno-mir-181a-2, rno-mir-181b-1, rno-mir-181b-2, rno-mir-181a-1, hsa-mir-449a, mmu-mir-449a, rno-mir-449a, mmu-mir-463, mmu-mir-466a, hsa-mir-483, hsa-mir-493, hsa-mir-181d, hsa-mir-499a, hsa-mir-504, mmu-mir-483, rno-mir-483, mmu-mir-369, rno-mir-493, rno-mir-369, rno-mir-374, hsa-mir-579, hsa-mir-582, hsa-mir-615, hsa-mir-652, hsa-mir-449b, rno-mir-499, hsa-mir-767, hsa-mir-449c, hsa-mir-762, mmu-mir-301b, mmu-mir-374b, mmu-mir-762, mmu-mir-344d-3, mmu-mir-344d-1, mmu-mir-673, mmu-mir-344d-2, mmu-mir-449c, mmu-mir-692-1, mmu-mir-692-2, mmu-mir-669b, mmu-mir-499, mmu-mir-652, mmu-mir-615, mmu-mir-804, mmu-mir-181d, mmu-mir-879, mmu-mir-297a-3, mmu-mir-297a-4, mmu-mir-344-2, mmu-mir-466b-1, mmu-mir-466b-2, mmu-mir-466b-3, mmu-mir-466c-1, mmu-mir-466e, mmu-mir-466f-1, mmu-mir-466f-2, mmu-mir-466f-3, mmu-mir-466g, mmu-mir-466h, mmu-mir-493, mmu-mir-504, mmu-mir-466d, mmu-mir-449b, hsa-mir-374b, hsa-mir-301b, rno-mir-466b-1, rno-mir-466b-2, rno-mir-466c, rno-mir-879, mmu-mir-582, rno-mir-181d, rno-mir-301b, rno-mir-463, rno-mir-673, rno-mir-652, mmu-mir-466l, mmu-mir-669k, mmu-mir-466i, mmu-mir-669i, mmu-mir-669h, mmu-mir-466f-4, mmu-mir-466k, mmu-mir-466j, mmu-mir-1193, mmu-mir-767, rno-mir-362, rno-mir-504, rno-mir-582, rno-mir-615, mmu-mir-3080, mmu-mir-466m, mmu-mir-466o, mmu-mir-466c-2, mmu-mir-466b-4, mmu-mir-466b-5, mmu-mir-466b-6, mmu-mir-466b-7, mmu-mir-466p, mmu-mir-466n, mmu-mir-344e, mmu-mir-344b, mmu-mir-344c, mmu-mir-344g, mmu-mir-344f, mmu-mir-374c, mmu-mir-466b-8, hsa-mir-466, hsa-mir-1193, rno-mir-449c, rno-mir-344b-2, rno-mir-466d, rno-mir-344a-2, rno-mir-1193, rno-mir-344b-1, hsa-mir-374c, hsa-mir-499b, mmu-mir-466q, mmu-mir-344h-1, mmu-mir-344h-2, mmu-mir-344i, rno-mir-344i, rno-mir-344g, mmu-let-7j, mmu-mir-30f, mmu-let-7k, mmu-mir-692-3, rno-let-7g, rno-mir-15a, rno-mir-762, mmu-mir-466c-3, rno-mir-29c-2, rno-mir-29b-3, rno-mir-344b-3, rno-mir-466b-3, rno-mir-466b-4
These miRNAs (miR-15a, miR-30, miR-182, and miR-804) are involved in cell proliferation, apoptosis, inflammation, epithelial-mesenchymal transition, invasion, oncogene inhibition, and intercellular adhesion. [score:3]
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24
[+] score: 3
In hippocampus, a total of 475 targets of rno-miR-101b-3p, rno-miR-217-5p, rno-miR-375-3p, rno-miR-20a-5p, rno-miR-19b-3p, and rno-miR-182 were predicted. [score:3]
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25
[+] score: 3
Moreover, altered expressions of miR-18a, miR-124, miR-343-3p, miR-16, miR-141, miR-182, and miR-200a in the brain tissue of suicidal patients have been reported [6]. [score:3]
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26
[+] score: 2
Guttilla et al. have shown that FOXO1 can be coordinately regulated by miR-27a, miR-96, and miR-182 38. [score:2]
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27
[+] score: 2
Other miRNAs from this paper: rno-mir-27a, rno-mir-130b, rno-mir-146a, rno-mir-200a
23, 32, 33 Several miRNAs, such as microRNA-130b, [34] microRNA-182, [35] microRNA-146a [36] and microRNA-200a, [37] have been found dysregulated in diabetes. [score:2]
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28
[+] score: 1
miR-182, of the miR-183 cluster family, is packaged in exosomes and is detected in human exosomes from serum, breast cells and prostate cells. [score:1]
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29
[+] score: 1
Similarly, the highest ranking “late” -induced miRNAs, including miR-203, miR-182, miR-181a, miR-369-3p, and miR-29c (Figure 6B), also make the greatest number of connections with the 12 genes analyzed in Figure 6B. [score:1]
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30
[+] score: 1
Recently, several other miRNAs including miR-24 and miR-182 was implicated to be important for insulin biosynthesis [20]. [score:1]
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31
[+] score: 1
At about E13, when the first waves of neurons are produced from neural progenitor cells in rat cortex [25], we found that 4 miRNAs were particularly high at this stage, including rno-miR-199a-3p, rno-miR-494, rno-miR-182, and rno-miR-7a, suggesting important roles of these miRNAs in neurogenesis. [score:1]
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32
[+] score: 1
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]
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33
[+] score: 1
MicroRNA-182 regulates amygdala -dependent memory formation. [score:1]
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34
[+] score: 1
Wu et al. [11] reported that the expression of certain miRNAs either increases (e. g., miR-182) or decreases (e. g., miR-10b) in parallel with DR progression in the retinas of rats with STZ -induced DM; however, no study has been conducted thus far to investigate miRNA variations in human retinal cells under prolonged HG exposure. [score:1]
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