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32 publications mentioning rno-mir-181b-2

Open access articles that are associated with the species Rattus norvegicus and mention the gene name mir-181b-2. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 281
MiR-181b targeted pirb mRNA to regulate PirB and its downstream signaling molecules after ischemic-reperfusion injuryTo determine whether miR-181b is associated with the expression of PirB and its downstream signaling molecules after ischemic-reperfusion injury, the effects of miR-181b mimics and miR-181b inhibitors on miR-181b expression in a mo del of OGD were detected in vitro. [score:10]
The results of these investigations increase the understanding of the mechanisms underlying the up-regulation of miR-181b expression and down-regulation of PirB expression by EA in the ischemic penumbra. [score:9]
These findings suggested that miR-181b up-regulation enhanced neurite growth by inhibiting PirB expression after OGD injury. [score:8]
The analyses showed that transfection of miR-181b mimics into neurons led to a decrease in PirB expression (P < 0.05); in contrast, transfection of miR-181b inhibitors significantly increased its expression (P < 0.05). [score:7]
To determine whether miR-181b is associated with the expression of PirB and its downstream signaling molecules after ischemic-reperfusion injury, the effects of miR-181b mimics and miR-181b inhibitors on miR-181b expression in a mo del of OGD were detected in vitro. [score:7]
Furthermore, these results provide the first evidence that EA directly regulates miR-181b expression following administration of miR-181b mimics or miR-181b inhibitors. [score:7]
One possible explanation for these findings is that miR-181b increased pirb mRNA and PirB protein expression to regulate the expression of downstream signaling molecules, such as RhoA and GAP43. [score:6]
These results demonstrated that miR-181b targeted pirb mRNA to regulate PirB expression. [score:6]
These results indicate that miR-181b targets pirb mRNA to regulate the expression of PirB and its downstream signaling molecules after ischemic-reperfusion injury. [score:6]
To test whether EA could enhance neurobehavioral functional recovery through regulating miR-181b expression and whether miR-181b could target pirb gene silencing after ischemic stroke, the rats received a subcutaneous Alzet osmotic minipump (Alzet, Cupertino, CA, USA) 45 46. [score:6]
Computational miRNA target analysis revealed that the pirb 3′-UTR was a predicted target of miR-181b. [score:5]
Interestingly, miRNA microarray analysis revealed that miR-181b expression was significantly decreased in the ischemic penumbra at 28 d post-MCAO, whereas enhanced its expression. [score:5]
The effect of miR-181b mimics or miR-181b inhibitors on PirB expression and neurite growth in vitro. [score:5]
These findings indicate that EA exerts its therapeutic effects on stroke by regulating epigenetic changes to directly act on its targets, such as the miR-181b/PirB/RhoA/GAP43 axis, which may be a novel mechanism underlying against ischemic stroke. [score:5]
org) to search for targets of miR-181b, we found that the 3′-UTR of pirb mRNA contains two putative miR-181b target sites (Fig. 4e). [score:5]
Post hoc analyses showed that or miR-181b mimic transfection decreased pirb mRNA and PirB protein expression at 28 d post-MCAO (P < 0.05; Fig. 5a–c); however, these effects were reversed by miR-181b inhibitor transfection (P < 0.05; Fig. 5a–c). [score:5]
The effect of miR-181b mimics or miR-181b inhibitors on PirB expression and neurite growth in vitroThe OGD mo del was used as above. [score:5]
Among these 20 miRNAs, miR-181b expression was markedly down-regulated in the MCAO group compared with the Sham group (Fig. 4a and b). [score:5]
Moreover, the decreased miR-181b expression inhibited neurite growth after OGD injury, which could be rescued by miR-181b mimics. [score:5]
Bar graph showing the relative expression of miR-181b normalized to the expression of the small RNA U6B (* P < 0.05 vs. [score:5]
The findings of this study indicate that EA exerts its therapeutic effects by inducing epigenetic changes to directly regulate its targets, such as the miR-181b/PirB/RhoA/GAP43 axis. [score:5]
These results suggest that miR-181b may directly regulate pirb mRNA expression and have a very important function in the treatment of cerebral ischemic-reperfusion injury using EA. [score:5]
Furthermore, increasing evidence shows that miR-181b governs axon specification and growth by regulating its target signaling molecules and plays an important role in the organization of neural connections 29 41. [score:4]
These results suggest that an increase in the brain-specific miR-181b level in the ischemic penumbra may be directly responsible for the mechanical repair of brain tissue, and they also imply that the rehabilitative effects of EA administration may include promoting miR-181b expression after cerebral ischemic injury. [score:4]
In contrast, the expression was higher in the OGD group and OGD+miR-181b inhibitors group compared with the Normal group at 72 h after OGD injury (P < 0.05; Fig. 6b and c). [score:4]
In conclusion, as shown in Fig. 7, this study first provides and verifies the solid evidences that enhances neurobehavioral functional recovery through miR-181b targeting PirB after ischemic stroke, suggesting that miR-181b and PirB act as key regulators of axon regeneration and CST projection after cerebral ischemic-reperfusion injury. [score:4]
EA enhances neurobehavioral functional recovery from ischemic stroke through a series of complex processes, which may include increasing the miR-181b level, decreasing PirB expression, and regulating the levels of PirB downstream signaling molecules (such as RhoA and GAP43). [score:4]
These results suggested that miR-181b regulated the expression of PirB and its downstream signaling molecules, thereby restricting neurite growth after ischemic injury. [score:4]
To explore the mechanisms of the miR-181b -mediated regulation of PirB expression and neurite growth, an OGD mo del was used. [score:4]
In contrast, decreased miR-181b expression was detected in the OGD+miR-181b inhibitors group compared with the Normal group (P < 0.05; Fig. 6a). [score:4]
These findings verify that PirB is a direct target of miR-181b and demonstrate that EA enhances neurobehavioral performance recovery through miR-181b -mediated pirb gene silencing after ischemic stroke. [score:4]
In contrast, RhoA expression increased in the OGD+miR-181b inhibitors group compared with the OGD+miR-181b mimics group (P < 0.05; Fig. 6f and g). [score:4]
The cultures were divided into groups as follows: Normal, OGD, OGD+ miR-181b mimics and OGD+ miR-181b inhibitors group. [score:3]
MiR-181b targeted pirb mRNA to regulate PirB and its downstream signaling molecules after ischemic-reperfusion injury. [score:3]
Cells were co -transfected with the firefly luciferase target reporter plasmid containing the pirb 3′-UTR (with either wild-type or mutated miR-181b binding sites), a Renilla luciferase control reporter, and miR-181b mimics or a negative control. [score:3]
MiR-181b, a member of the miR-181 family, is expressed at intriguingly high levels in the retina and brain areas associated with motor function 29. [score:3]
The effects of miR-181b on PirB, RhoA and GAP43 expression after OGD injury. [score:3]
Luciferase assay further demonstrated that PirB was likely a direct target of miR-181b. [score:3]
Each pump contained sterile 0.9% saline with miR-181b mimics or miR-181b inhibitors in dimethylsulfoxide (DMSO), which were administered to the animals continuously until the study end (delivering 2 ng/day for 28 days). [score:3]
Our results also showed that and miR-181b mimic administration had similar effects on pirb mRNA and PirB protein expression. [score:3]
In contrast, GAP43 expression increased in the OGD+miR-181b mimics group compared with the OGD group (P < 0.05; Fig. 6h and i), and decreased in the OGD+miR-181b inhibitors group compared with the OGD+miR-181b mimics group (P < 0.05; Fig. 6h and i). [score:3]
These results suggested that EA enhanced neurobehavioral functional recovery by promoting the targeting of pirb mRNA by miR-181b after ischemic stroke. [score:3]
However, miR-181b inhibitor transfection altered the effects of EA or the miR-181b mimics on the rota-rod and grip strength performances (P < 0.05; Fig. 5e and f). [score:3]
To further elucidate the underlying molecular mechanisms of EA-produced neurobehavioral functional recovery, we searched for a possible relationship between miR-181b and pirb mRNA, which may be the miR-181b target that participates in this process. [score:3]
The miR-181b mimics or miR-181b inhibitors were purchased from GenePharma. [score:3]
After rehabilitation of sugar-oxygen, miR-181b mimics or inhibitors were added using Lipofectamine 2000 (Invitrogen) according to the manufacturer’s instructions. [score:3]
In contrast, the miR-181b inhibitors increased the pirb mRNA and PirB protein levels. [score:3]
Furthermore, mimics or inhibitors of miR-181b were transfected into the primary neuron cultures. [score:3]
Next, we assessed the effects of miR-181b mimics and miR-181b inhibitors on pirb mRNA in the mo del of OGD. [score:3]
The expression of miR-181b, pirb mRNA and PirB protein were also performed at 28 d after reperfusion. [score:3]
We examined the effects of miR-181b on pirb mRNA and PirB protein expression in the ischemic penumbra after stroke. [score:3]
How to cite this article: Deng, B. et al. Electroacupuncture enhances rehabilitation through miR-181b targeting PirB after ischemic stroke. [score:3]
Next, miR-181b expression in the ischemic penumbra was examined. [score:3]
Next, miR-181b mimics or miR-181b inhibitors were transfected into cerebral cortex neurons in the ischemic penumbra. [score:3]
The cells were co -transfected with 0.2 μg of a firefly luciferase target reporter plasmid, the pMIR-REPORT PirB 3′-UTR plasmid (with either wild-type or mutated miR-181b -binding sites), 0.01 μg of a Renilla luciferase control reporter, and 100 nM miRNA mimics or negative control using Lipofectamine2000 (Invitrogen, California, USA), according to the manufacturer’s instructions. [score:3]
The pirb mRNA and miR-181b expression were tested by qRT-PCR analysis. [score:3]
Post hoc analyses showed that or miR-181b mimic transfection increased the miR-181b level at 28 d post-MCAO (P<0.05; Fig. 5i); however, this effect was reversed by miR-181b inhibitor transfection (P < 0.05; Fig. 5i). [score:3]
The mNSS of the MCAO + EA group and MCAO+miR-181b mimics group were significantly lower than that of the MCAO group at 28 d after reperfusion (P < 0.05); this effect was reversed by miR-181b inhibitor transfection (P < 0.05; Fig. 5d). [score:3]
EA enhanced neurobehavioral functional recovery through miR-181b -mediated pirb gene silencing after ischemic strokeWe examined the effects of miR-181b on pirb mRNA and PirB protein expression in the ischemic penumbra after stroke. [score:3]
Rats which had been operated successfully were randomly divided into the following groups: Sham, MCAO, MCAO + EA group, MCAO + EA group+miR-181b inhibitors, MCAO+ miR-181b mimics (n = 6 for each group). [score:3]
In contrast, its level was lower in the miR-181b inhibitors group compared with that in the Normal group (P < 0.05; Fig. 5h). [score:2]
At 72 h after OGD, Then the expression of miR-181b, pirb mRNA, PirB protein, RhoA, GAP43, β-actin and average length of the longest neurites assay were tested as above. [score:2]
In addition, significantly increased miR-181b expression was observed in the OGD+miR-181b mimics group compared with the OGD group (P < 0.05; Fig. 6a). [score:2]
These results demonstrate that EA can regulate the miR-181b level in the ischemic penumbra after stroke. [score:2]
In contrast, the neurite length was significantly reduced in the OGD+miR-181b inhibitors group compared with the OGD+miR-181b mimics group (P < 0.05). [score:2]
However, its expression decreased in the OGD+miR-181b mimics group compared with the OGD group (P < 0.05; Fig. 6f and g). [score:2]
To determine whether the pirb mRNA is potentially regulated by miR-181b, we constructed a reporter plasmid by inserting the cDNA corresponding to the 3′-UTR of pirb mRNA into the 3′region of the firefly luciferase gene. [score:2]
MCAO group) (h) Evaluation the effects of miR-181b mimics and inhibitors on the miR-181b level in primary neurons in vitro. [score:1]
EA increased the miR-181b level in the rat ischemic penumbra after stroke. [score:1]
However, the role of miR-181b in the ischemic penumbra in association with for stroke remains to be elucidated. [score:1]
EA enhanced neurobehavioral functional recovery through miR-181b -mediated pirb gene silencing after ischemic stroke. [score:1]
To the best of our knowledge, our study is the first to demonstrate a decrease in the miR-181b level at 72 h after OGD injury. [score:1]
Post hoc analyses showed miR-181b level had no remarkable difference in every group at 1 h before MCAO surgery (P > 0.05). [score:1]
EA increased the miR-181b level in ischemic penumbra after stroke. [score:1]
To perform qRT-PCR of miR-181b, a small RNA fraction was isolated with a mirVana miRNA Isolation Kit (Genetimes Technology, Inc. [score:1]
In particular, the relevance of miR-181b function to the organization of neural connections has been reported and identified. [score:1]
Post hoc analyses showed miR-181b level in the miR-181b mimics group was higher than that in the Normal group (P < 0.05; Fig. 5h). [score:1]
Post hoc analyses showed miR-181b caused a significant decrease in luciferase activity (P < 0.05; Fig. 4f), whereas they did not alter the luciferase activity in cells transfected with reporter constructs containing a mutated miR-181b 3′-UTR. [score:1]
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2
[+] score: 205
After SAP induction by taurocholate and the treatment with Panax notoginseng saponins for 24 h, we detected the up-regulated miR-181b, the reduced Bcl-2 expression, the increased activity of mTOR/Akt, the blocked Beclin1 and LC3-II expressions, and the enhanced Caspase-3 expression. [score:10]
The changes suggested that PNS could suppress the expressions of Akt, Beclin1 and LC3-II, and upregulate miR-181b and mTOR expressions (Figs.   5– 6). [score:10]
PNS showed a protective effect on taurocholate -induced SAP and exerted a therapeutic effect through upregulating the miR-181b expression, decreasing the activity of mTOR/Akt pathway, attenuating Beclin1 and LC3-II expressions, enhancing the activity of caspase-3 pathway, increasing pancreatic cell apoptosis, reducing autophagy, ameliorating the impaired intestinal mucosal barrier, attenuating taurocholate -induced pancreatic damage, and increasing the survival rate in taurocholate -induced SAP rats. [score:8]
The study results suggested that overexpression of miR-181b protected taurocholate -induced AP by inhibiting autophagy apoptosis and promoting autophagy via regulating Beclin1 and LC3-II expression. [score:8]
To explore the effects of miR-181b on Beclin1 and LC3-II expressions, we transfected AR42J cells with MiR-181b mimics, MiR-181b mimic -negative control (NC), miR-181b inhibitor, or miR-181b inhibitor-NC. [score:7]
In the study, administration of PNS significantly decreased Blc-2 expression and increased caspase-3 expression by increasing miR-181b expression, promoting pancreatic acinar cell apoptosis, and reducing taurocholate -induced pancreatic injury. [score:7]
To further investigate the effects of miR-181b on taurocholate induced-AP, we injected AdCMV-miR-181b into rats by tail intravenous administration, followed by intraperitoneal taurocholate challenge in 10 days, and found that the overexpression of miR-181b inhibited Beclin1 and LC3-II expression, reduced autophagy, and inhibited pancreatic damage in rats with taurocholate -induced AP. [score:7]
In the study, PNS treatment ameliorated sodium taurocholate -induced pancreatitis by increasing apoptosis and inhibiting autophagy, suggesting that PNS might have the application potential in the treatment of pancreatitis by regulating miR-181b expression. [score:6]
In the study, miR-181b expression was significantly down-regulated in the AP mo del. [score:6]
These results suggested that miR-181b might inhibit autophagy and regulate Beclin1 and LC3-II expressions. [score:6]
Overexpression of miR-181b inhibited pancreatic damage in the rats with SAP induced by taurocholate. [score:5]
MiR-181b mimics, MiR-181b mimic -negative control (NC), miR-181b inhibitor, or miR-181b inhibitor-NC (Invitrogen, Carlsbad, CA, USA) were mixed with Lipofectamine 2000 (Invitrogen), and then added into the culture medium. [score:5]
MiR-181b mimics, miR-181b mimic -negative control (NC), miR-181b inhibitor, and miR-181b inhibitor-NC were transfected in AR42J cells and Beclin1 and LC3-II expressions were measured by western blotting. [score:5]
Fig. 4Effects of overexpression of miR-181b on LC3-II and Beclin1 expressions in rats with SAP induced by taurocholate. [score:5]
Overexpression of miR-181b decreased Beclin1 and LC3-II expressions in rats with SAP induced by taurocholate. [score:5]
Therefore, the downregulation of miR-181b might affect pancreas tissues in AP by regulating the activity of the mTOR/Akt pathway. [score:5]
MiR-181b significantly down-regulated Beclin1 and LC3-II expression in AR42J cells. [score:5]
However, the administration of PNS increased the activity of mTOR and miR-181b, inhibited Beclin1 and LC3-II expression, decreased pancreatic cell autophagy, enhanced pancreatic cell apoptosis, and ameliorated taurocholate -induced AP. [score:5]
In taurocholate -induced rats, the mRNA and proteins of miR-181 and mTOR were significantly decreased (P < 0.05) and Akt, Beclin1 and LC3-II expressions were significantly upregulated compared to the control group (P < 0.05). [score:5]
the control group To analyze the effects of overexpression of miR-181b on Beclin1 and LC3-II expression in rats with taurocholate -induced acute pancreatitis, we performed western blotting on pancreatic tissue samples. [score:5]
The increase in miR-181b expression significantly decreased Beclin1 and LC3-II expressions in the miR-181b mimics group compared to the control group and all treatment groups (P < 0.05) (Fig.   2). [score:4]
After PNS treatment, the expressions of miR-181 and mTOR were markedly enhanced (P < 0.05), whereas Akt, Beclin1, and LC3-II expressions were significantly lower compared to the SAP group (P < 0.05). [score:4]
However, overexpression of miR-181b in rats with taurocholate -induced AP (the SAP/miR-181b group) resulted in the decreased Beclin1 and LC3-II expressions compared to the rats induced by taurocholate (SAP group) (P < 0.05). [score:4]
By up -regulating the miR-181b expression level, Panax notoginseng saponins significantly reduced taurocholate -induced pancreas injury and autophagy and increased apoptosis. [score:4]
Fig. 5Effects of PNS on the expressions of miR-181b, mTOR, Akt, Beclin1, and LC3-II mRNA in pancreas tissues from the rats with SAP induced by taurocholate. [score:3]
MiR-181a and miR-181b of the miR-181 family are tumor suppressors for inducing apoptosis [57]. [score:3]
However, the contribution of miRNA-181b in autophagy-related diseases, especially AP, is still unclear. [score:3]
Moreover, PNS increased the activity of miR-181b, stimulated the activity of the mTOR/Akt pathway, decreased LC3-II and Beclin1 expressions, reduced the number of phagophores, autophagosomes and autolysosomes, reduced autophagy, and ameliorated taurocholate -induced AP. [score:3]
Fig. 2Effects of miR-181b on Beclin1 and LC3-II expressions in AR42J cells. [score:3]
Fig. 3Effects of overexpression of miR-181b on pancreas damage in the rats with SAP induced by taurocholate. [score:3]
The constitutively active miR-181b expression construct was delivered to rats by intravenous administration of 1 × 10 [9] PFU of AdCMV-miR-181b at 10 d, at the time of taurocholate -induced pancreatitis. [score:3]
Effects of PNS on the expressions of miR-181b, mTOR, Akt, Beclin1 and LC3-II in taurocholate -induced pancreas tissue. [score:3]
controls and all treatment groups To analyze the effects of overexpression of miR-181b on pancreatic damage in rats with taurocholate -induced SAP, we injected 1 × 10 [9] PFU of AdCMV-miR-181b into rats by tail intravenous administration, followed by intraperitoneal taurocholate challenge in 10 days. [score:3]
a Images of hematoxylin and eosin-stained pancreas sections from SO group, SAP group and miR-181b -expressing group. [score:3]
Moreover, miR-181 significantly enhanced drug -induced apoptosis in cancer cells by targeting multiple anti-apoptosis genes, such as Bcl-2 [57, 58]. [score:3]
Our data suggested that taurocholate -induced AP decreased the activity of miR-181b, stimulated the activity of the PI3K/Akt signaling pathway, attenuated the activity of mTOR pathway, enhanced Beclin1 and LC3-II expression, and increased pancreatic cell autophagy, pancreatic cell apoptosis, and taurocholate -induced AP. [score:3]
Whether miR-181b functions as an autophagy and apoptosis-responsive miRNA to regulate the pancreatitis response to autophagy by regulating mTOR/Akt and apoptosis signaling pathway is still unknown. [score:3]
These effects may be mediated by inducing miR-181b and mTOR expressions in pancreas and subsequently reducing autophagosome formation, which is important for initiating pancreatitis [40– 42]. [score:3]
MiR-181b might play a significant role in AP biology and represent an interesting new therapeutic target for AP. [score:2]
Histopathological examination of the pancreas of taurocholate -treated miR-181b -expressing rats revealed the markedly extenuated pancreatic damage compared with control animals (Fig.   3). [score:2]
We hypothesized that miR-181b played an important role in the development of AP. [score:2]
As shown in Fig.   4, taurocholate -induced SAP tissues in SAP/miR-181b group and SAP group showed the significantly increased Beclin1 and LC3-II expressions compared to the SO group and SO/miR-181b group (P < 0.05). [score:2]
Furthermore, we transfected AR42J cells with miR-181b mimics and indicated that Beclin1 and LC3-II expressions were significantly decreased compared with the control group and all treatment groups (P < 0.05). [score:2]
MiR-181 induced apoptosis in astrocytes by targeting multiple members of the Bcl-2 family [58]. [score:2]
The expressions of LC3-II and Beclin1 in the SO group, SO miR-181b group, SAP group and SAP miR-181b group were measured via Western Blot analysis. [score:1]
After 24 h, the expression levels of miR-181b, Beclin1, LC3-II, Akt and mTOR from pancreas tissues were measured by Western Blotting and RT-PCR. [score:1]
Tail intravenous administration of AdCMV-miR-181b. [score:1]
Acute pancreatitis Panax notoginseng saponins miR-181b Taurocholate Rat As an abdominal emergency, acute pancreatitis (AP) involves concomitant organ failures and other eventful complications and generally causes considerable deaths [1]. [score:1]
The miR-181 family of miRNAs is a broadly conserved group of miRNAs and its members affect cell proliferation, differentiation and death [27, 28]. [score:1]
AdCMV-miR-181b was constructed as previously described [32, 33]. [score:1]
Rats were injected with AdCMV-miR-181b by tail intravenous administration, followed by intraperitoneal taurocholate challenge in 10 days. [score:1]
a RT-PCR results of miR-181b, LC3-II, mTOR, Akt, Beclin1, and mRNA in the SO group, SAP group and PNS treatment group. [score:1]
the normal control group We evaluated the effects of PNS treatment on SAP rats by examining the expressions of miR-181b, mTOR, Akt, Beclin1 and LC3-II in taurocholate -induced pancreas tissue by RT-PCR and Western Blotting. [score:1]
In the SAP mo del, we found that taurocholate -induced AP decreased the activity of miR-181b and increased the activity of the mTOR/Akt pathway. [score:1]
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3
[+] score: 28
The miR-181 family is particularly enriched in the brain and is involved in autism spectrum disorders [56], schizophrenia [57], Alzheimer disease [58], where they are mainly found to be upregulated. [score:6]
Note that prenatal stress downregulated miR-181 and miR-186 expression in the frontal cortex. [score:6]
Downregulation of miR-181 contributes to accelerated HIV -associated dementia in opiate abusers [59]. [score:4]
Behavioural findings in stressed dams were accompanied by altered epigenetic profiles in the frontal cortex, including downregulation of miR-181b. [score:4]
Downregulation of miR-181 was shown to have protective effects against apoptosis and mitochondrial dysfunction [60]. [score:4]
At the cellular level, miR-181 regulates apoptosis factors such as bcl-2 in astrocytes. [score:2]
miR-181 and miR-186 were chosen for verification using qRT-PCR analysis. [score:1]
Stress also led to critical decreases in let-7c, miR-23b, miR-181, and miR186 amounts. [score:1]
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4
[+] score: 26
Amongst these, miR-383 was differentially expressed in all three rats and up-regulated to the largest degree in rat one, and the ten other miRNAs, let-7d*, miR-181b, miR-187, miR-195, miR-214, miR-382, miR-411, miR-466b, miR-592 and miR-1224 were differentially expressed in at least two rats. [score:8]
In these 10 deregulated miRNAs, seven (let-7d*, miR-181b, miR-187, miR-214, miR-466b, miR-592, miR-1224) are up-regulated in two rats, and one (miR-195) is down-regulated. [score:8]
Hence, miR-383 was differentially expressed in three rats, and let-7d*, miR-181b, miR-187, miR-195, miR-214, miR-382, miR-411, miR-466b, miR-592, miR-1224 were differentially expressed in two rats at least (Additional file 2: Table S4). [score:5]
In dysregulated miRNAs, let-7d*, miR-181b, miR-187, miR-214, miR-383, miR-466b, miR-592, miR-1224 are significantly overexpressed in MrD compared to hippocampus, and miR-195 is downexpressed. [score:5]
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5
[+] score: 18
Other miRNAs from this paper: rno-mir-31a, rno-mir-181b-1, rno-mir-31b, rno-mir-291b, rno-mir-155
Chronic ethanol feeding decreases the expression of miRNA181b-3p, which in turn upregulates the expression of the nuclear-cytoplasmic shuttling protein, importin α5, contributing to increased p65 translocation to the nucleus in Kupffer cells after chronic ethanol feeding [8]. [score:8]
Focusing on miRNAs whose expression is decreased by ethanol revealed that chronic ethanol enhanced a miR181b-3p → importin α5 regulatory axis in hepatic macrophages that contributed to the sensitization of TLR4 -dependent cytokine expression in these Kupffer cells. [score:6]
Through normalization of expression miR291b, as well as miR181b-3p [8], treatment of HA35 protected from the effects of ethanol in Kupffer cells and PBMCs from patients with AH, suggesting that HA35 has potential as a therapeutic agent for the treatment of ALD. [score:3]
These data add to a growing number of miRNAs involved in the response to macrophages to ethanol, including miR155 [23] and miR181b-3p [8]. [score:1]
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6
[+] score: 13
Interestingly, miR-9, miR-124a, miR-99a/b and miR-181b/c up-regulation during early cortical neurogenesis was negatively correlated with the expression level of their predicted targets, consistent with reports that have found a negative expression correlation between tissue-enriched miRNAs and their putative targets [17, 18]. [score:12]
These include miR-7, miR-9, miR-124a, miR-125a/b, miR-181b/c and miR-99a/b. [score:1]
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7
[+] score: 9
Conversely, changes in microRNA expression may reduce the activation of the inflammatory NF-κB Ρpathway; for example, this may have occurred via the decreased expression of miR-124 and miR-181b at 3 and 7 days after injury and the increased expression of miR-15, miR-223 and miR-146a (Table 8). [score:7]
Specifically, miR-Let7a, miR-107, and miR-183 have been described as regulators of cell death, and miR-181b and miR199 are involved in the control of inflammation (see file S6). [score:2]
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8
[+] score: 9
Among the important genes were Lifr, Acvr1c, and Pparγ which were found to be targeted by microRNAs in our dataset like miR-143, miR-30, miR-140, miR-27b, miR-125a, miR-128ab, miR-342, miR-26ab, miR-181, miR-150, miR-23ab and miR-425. [score:3]
Both miR-27b and miR-181b were among the most downregulated microRNAs in parous compared to nulliparous ALDH positive MECs. [score:3]
It was found to be a putative target for let-7 family members, miR-26ab, miR-181 family, miR-150, miR-27b, miR-23ab, miR-425, miR-125a-5p, and miR-128ab. [score:3]
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9
[+] score: 8
miRNA Target Genes Pathways miR-128 ABCB9, BTG1, DSCR1, RASD1 ABC transporters General miR-136 GRN, PPP1R9B miR-147 HOXA1, PTGFRN miR-148 EGR3, SCN3A miR-181b IGF1R, NKX6-1 Adherens junction, Maturity onset diabetes of the, Focal adhesion, **Long term depression miR-196a ABCB9, CPB2, IRS1, MAPK10 ABC transporters General, Complement and coagulation cas, Adipocytokine signaling pathwa, Insulin signaling pathway, Type II diabetes mellitus, Fc epsilon RI signaling pathwa, Focal adhesion, **GnRH signaling pathway, **MAPK signaling pathway, Toll like receptor signaling p, Wnt signaling pathway miR-203 SARA1 miR-20 BTG1, SARA1, YWHAB Cell cycle miR-21 TPM1 mir-216 GNAZ **Long term depression miR-217 RHOA Adherens junction, Axon guidance, Focal adhesion, Leukocyte transendothelial mig, Regulation of actin cytoskelet, TGF beta signaling pathway, T cell receptor signaling path, Tight junction, Wnt signaling pathway miR-31 ATP2B2, DNM1L, EGR3, PPP1R9B, YWHAB **Calcium signaling pathway, Cell cycle miR-7 SLC23A2 miR-7b HRH3, NCDN, SLC23A2 **Neuroactive ligand receptor in b: miRNAs and their targets (from TargetScan and miRanda). [score:8]
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10
[+] score: 7
miRNAs that had approximately 2-fold upregulation included members of miR-29 family and miR-34 family and that were downregulated by about 2-fold were members of the miR-181 family and miR-183 family. [score:7]
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[+] score: 7
HMGA1 enhances the expression of miR-181b, which in turn, represses the translation of CBX7 mRNA. [score:5]
Interestingly, in breast carcinoma, HMGA1 takes part in an important regulatory circuitry involving CBX7 and miR-181b microRNA (miRNA) (34) (Figure 1A). [score:2]
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[+] score: 6
Other miRNAs from this paper: mmu-mir-1a-1, mmu-mir-127, mmu-mir-134, mmu-mir-136, mmu-mir-154, mmu-mir-181a-2, mmu-mir-143, mmu-mir-196a-1, mmu-mir-196a-2, mmu-mir-21a, rno-mir-329, mmu-mir-329, mmu-mir-1a-2, mmu-mir-181a-1, mmu-mir-181b-1, mmu-mir-181c, mmu-mir-375, mmu-mir-379, mmu-mir-181b-2, rno-mir-21, rno-mir-127, rno-mir-134, rno-mir-136, rno-mir-143, rno-mir-154, rno-mir-181c, rno-mir-181a-2, rno-mir-181b-1, rno-mir-196a, rno-mir-181a-1, mmu-mir-196b, rno-mir-196b-1, mmu-mir-412, mmu-mir-370, oar-mir-431, oar-mir-127, oar-mir-432, oar-mir-136, mmu-mir-431, mmu-mir-433, rno-mir-431, rno-mir-433, ssc-mir-181b-2, ssc-mir-181c, ssc-mir-136, ssc-mir-196a-2, ssc-mir-21, rno-mir-370, rno-mir-412, rno-mir-1, mmu-mir-485, mmu-mir-541, rno-mir-541, rno-mir-493, rno-mir-379, rno-mir-485, mmu-mir-668, bta-mir-21, bta-mir-181a-2, bta-mir-127, bta-mir-181b-2, bta-mir-181c, mmu-mir-181d, mmu-mir-493, rno-mir-181d, rno-mir-196c, rno-mir-375, mmu-mir-1b, bta-mir-1-2, bta-mir-1-1, bta-mir-134, bta-mir-136, bta-mir-143, bta-mir-154a, bta-mir-181d, bta-mir-196a-2, bta-mir-196a-1, bta-mir-196b, bta-mir-329a, bta-mir-329b, bta-mir-370, bta-mir-375, bta-mir-379, bta-mir-412, bta-mir-431, bta-mir-432, bta-mir-433, bta-mir-485, bta-mir-493, bta-mir-541, bta-mir-181a-1, bta-mir-181b-1, ssc-mir-1, ssc-mir-181a-1, mmu-mir-432, rno-mir-668, ssc-mir-143, ssc-mir-181a-2, ssc-mir-181b-1, ssc-mir-181d, ssc-mir-196b-1, ssc-mir-127, ssc-mir-432, oar-mir-21, oar-mir-181a-1, oar-mir-493, oar-mir-433, oar-mir-370, oar-mir-379, oar-mir-329b, oar-mir-329a, oar-mir-134, oar-mir-668, oar-mir-485, oar-mir-154a, oar-mir-154b, oar-mir-541, oar-mir-412, mmu-mir-21b, mmu-mir-21c, ssc-mir-196a-1, ssc-mir-196b-2, ssc-mir-370, ssc-mir-493, bta-mir-154c, bta-mir-154b, oar-mir-143, oar-mir-181a-2, chi-mir-1, chi-mir-127, chi-mir-134, chi-mir-136, chi-mir-143, chi-mir-154a, chi-mir-154b, chi-mir-181b, chi-mir-181c, chi-mir-181d, chi-mir-196a, chi-mir-196b, chi-mir-21, chi-mir-329a, chi-mir-329b, chi-mir-379, chi-mir-412, chi-mir-432, chi-mir-433, chi-mir-485, chi-mir-493, rno-mir-196b-2, bta-mir-668, ssc-mir-375
For example, miR-273 and the lys-6 miRNA have been shown to be involved in the development of the nervous system in nematode worm [3]; miR-430 was reported to regulate the brain development of zebrafish [4]; miR-181 controlled the differentiation of mammalian blood cell to B cells [5]; miR-375 regulated mammalian islet cell growth and insulin secretion [6]; miR-143 played a role in adipocyte differentiation [7]; miR-196 was found to be involved in the formation of mammalian limbs [8]; and miR-1 was implicated in cardiac development [9]. [score:6]
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[+] score: 6
The inhibitory effects of miR-466 on Prox1 expression, tube formation, and lymphatic vessel formation were comparable to those of miR-181. [score:5]
MicroRNA Prox1 miR-466 miR-181 Tube Formation Lymphangiogenesis Cornea transplantation Alkali burn Approximately 10%–50% of cornea transplantation recipients experience graft rejection within one year [1]. [score:1]
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14
[+] score: 6
Other evidence suggests that overexpression of miR-181b increases the growth of HSCs by directly targeting p27 [39]. [score:6]
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15
[+] score: 5
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-16-1, hsa-mir-17, hsa-mir-18a, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-20a, hsa-mir-22, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-98, hsa-mir-101-1, hsa-mir-16-2, mmu-let-7g, mmu-let-7i, mmu-mir-1a-1, mmu-mir-15b, mmu-mir-101a, mmu-mir-126a, mmu-mir-130a, mmu-mir-133a-1, mmu-mir-142a, mmu-mir-181a-2, mmu-mir-194-1, hsa-mir-208a, hsa-mir-30c-2, mmu-mir-122, mmu-mir-143, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-181a-1, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-15b, hsa-mir-122, hsa-mir-130a, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-142, hsa-mir-143, hsa-mir-126, hsa-mir-194-1, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-208a, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-15a, mmu-mir-16-1, mmu-mir-16-2, mmu-mir-18a, mmu-mir-20a, mmu-mir-22, mmu-mir-26a-1, mmu-mir-26b, mmu-mir-29c, mmu-mir-98, mmu-mir-326, rno-mir-326, rno-let-7d, rno-mir-20a, rno-mir-101b, mmu-mir-101b, hsa-mir-1-1, mmu-mir-1a-2, hsa-mir-181b-2, mmu-mir-17, mmu-mir-19a, mmu-mir-181a-1, mmu-mir-26a-2, mmu-mir-19b-1, mmu-mir-181b-1, mmu-mir-181c, hsa-mir-194-2, mmu-mir-194-2, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-101-2, hsa-mir-26a-2, hsa-mir-378a, mmu-mir-378a, hsa-mir-326, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, mmu-mir-181b-2, rno-let-7a-1, rno-let-7a-2, rno-let-7b, rno-let-7c-1, rno-let-7c-2, rno-let-7e, rno-let-7f-1, rno-let-7f-2, rno-let-7i, rno-mir-15b, rno-mir-16, rno-mir-17-1, rno-mir-18a, rno-mir-19b-1, rno-mir-19a, rno-mir-22, rno-mir-26a, rno-mir-26b, rno-mir-29c-1, rno-mir-30c-1, rno-mir-30c-2, rno-mir-98, rno-mir-101a, rno-mir-122, rno-mir-126a, rno-mir-130a, rno-mir-133a, rno-mir-142, rno-mir-143, rno-mir-181c, rno-mir-181a-2, rno-mir-181b-1, rno-mir-194-1, rno-mir-194-2, rno-mir-208a, rno-mir-181a-1, hsa-mir-423, hsa-mir-18b, hsa-mir-20b, hsa-mir-451a, mmu-mir-451a, rno-mir-451, ssc-mir-122, ssc-mir-15b, ssc-mir-181b-2, ssc-mir-19a, ssc-mir-20a, ssc-mir-26a, ssc-mir-326, ssc-mir-181c, ssc-let-7c, ssc-let-7f-1, ssc-let-7i, ssc-mir-18a, ssc-mir-29c, ssc-mir-30c-2, hsa-mir-484, hsa-mir-181d, hsa-mir-499a, rno-mir-1, rno-mir-133b, mmu-mir-484, mmu-mir-20b, rno-mir-20b, rno-mir-378a, rno-mir-499, hsa-mir-378d-2, mmu-mir-423, mmu-mir-499, mmu-mir-181d, mmu-mir-18b, mmu-mir-208b, hsa-mir-208b, rno-mir-17-2, rno-mir-181d, rno-mir-423, rno-mir-484, mmu-mir-1b, ssc-mir-15a, ssc-mir-16-2, ssc-mir-16-1, ssc-mir-17, ssc-mir-130a, ssc-mir-101-1, ssc-mir-101-2, ssc-mir-133a-1, ssc-mir-1, ssc-mir-181a-1, ssc-let-7a-1, ssc-let-7e, ssc-let-7g, ssc-mir-378-1, ssc-mir-133b, ssc-mir-499, ssc-mir-143, ssc-mir-423, ssc-mir-181a-2, ssc-mir-181b-1, ssc-mir-181d, ssc-mir-98, ssc-mir-208b, ssc-mir-142, ssc-mir-19b-1, hsa-mir-378b, ssc-mir-22, rno-mir-126b, rno-mir-208b, rno-mir-133c, hsa-mir-378c, ssc-mir-194b, ssc-mir-133a-2, ssc-mir-484, ssc-mir-30c-1, ssc-mir-126, ssc-mir-378-2, ssc-mir-451, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, mmu-mir-378b, mmu-mir-101c, hsa-mir-451b, hsa-mir-499b, ssc-let-7a-2, ssc-mir-18b, hsa-mir-378j, rno-mir-378b, mmu-mir-133c, mmu-let-7j, mmu-mir-378c, mmu-mir-378d, mmu-mir-451b, ssc-let-7d, ssc-let-7f-2, ssc-mir-20b-1, ssc-mir-20b-2, ssc-mir-194a, mmu-let-7k, mmu-mir-126b, mmu-mir-142b, rno-let-7g, rno-mir-15a, ssc-mir-378b, rno-mir-29c-2, rno-mir-1b, ssc-mir-26b
Our study revealed miR-181 and miR-142-3p with relatively high expression in thymus (Figure 2C), and miR18a and miR-20a appeared to be weakly expressed in thymus (Figure 2D). [score:5]
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[+] score: 5
Male-biased miRNA expression was associated with pathways related to cancer (miR-130b, miR-214, miR-181b, miR-199a, miR-150, miR-135a, miR-142-3p, miR-142-5p, miR-185), hematological disease (miR-22*, miR-142-3p, miR-142-5p, miR-150, miR-181b), and renal inflammation/nephritis (miR-130b, miR-223, miR-150, miR-142-5p, miR-296*, miR-185-3p) (Additional file 2). [score:5]
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[+] score: 4
Pathway and signaling pathway analyses demonstrated that miR-181 targets genes encoding antioxidant enzymes, including glutathione peroxidases 1 and 4 (Gpx1 and Gpx4, resp. ) [score:3]
Hutchison et al. used microarray analysis to assess the effects of miR-181 on the transcriptome in primary astrocytes. [score:1]
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[+] score: 4
Other miRNAs from this paper: cel-let-7, cel-lin-4, 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-17, hsa-mir-29a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-101-1, hsa-mir-29b-1, hsa-mir-29b-2, mmu-let-7g, mmu-let-7i, mmu-mir-29b-1, mmu-mir-101a, mmu-mir-128-1, mmu-mir-9-2, mmu-mir-132, mmu-mir-138-2, mmu-mir-181a-2, mmu-mir-199a-1, hsa-mir-199a-1, hsa-mir-7-1, hsa-mir-7-2, hsa-mir-7-3, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-199a-2, hsa-mir-181a-1, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-128-1, hsa-mir-132, hsa-mir-138-2, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-138-1, 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-29a, mmu-mir-29c, mmu-mir-92a-2, rno-let-7d, rno-mir-7a-1, rno-mir-101b, mmu-mir-101b, hsa-mir-181b-2, mmu-mir-17, mmu-mir-181a-1, mmu-mir-29b-2, mmu-mir-199a-2, mmu-mir-92a-1, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-138-1, mmu-mir-181b-1, mmu-mir-181c, mmu-mir-128-2, hsa-mir-128-2, mmu-mir-7a-1, mmu-mir-7a-2, mmu-mir-7b, hsa-mir-29c, hsa-mir-101-2, cel-lsy-6, mmu-mir-181b-2, rno-let-7a-1, rno-let-7a-2, rno-let-7b, rno-let-7c-1, rno-let-7c-2, rno-let-7e, rno-let-7f-1, rno-let-7f-2, rno-let-7i, rno-mir-7a-2, rno-mir-7b, rno-mir-9a-1, rno-mir-9a-3, rno-mir-9a-2, rno-mir-17-1, rno-mir-29b-2, rno-mir-29a, rno-mir-29b-1, rno-mir-29c-1, rno-mir-92a-1, rno-mir-92a-2, rno-mir-101a, rno-mir-128-1, rno-mir-128-2, rno-mir-132, rno-mir-138-2, rno-mir-138-1, rno-mir-181c, rno-mir-181a-2, rno-mir-181b-1, rno-mir-199a, rno-mir-181a-1, rno-mir-421, hsa-mir-181d, hsa-mir-92b, hsa-mir-421, mmu-mir-181d, mmu-mir-421, mmu-mir-92b, rno-mir-17-2, rno-mir-181d, rno-mir-92b, rno-mir-9b-3, rno-mir-9b-1, rno-mir-9b-2, mmu-mir-101c, mmu-let-7j, mmu-let-7k, rno-let-7g, rno-mir-29c-2, rno-mir-29b-3, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
Examination of the temporal clusters revealed that probes with similar sequences showed correlated expression, as exemplified by miR-181a, miR-181b, miR-181c, smallRNA-12 (Figure 4a) and miR-29a, miR-29b and miR-29c (Figure 4b), respectively. [score:3]
The mouse microRNA miR-181 has been implicated in the modulation of hematopoietic differentiation, and other mammalian microRNAs have been suggested to play roles in cancer [22, 23]. [score:1]
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[+] score: 4
Some researchers ever reported that miR-21 and miR-181 were significantly upregulated post-MI [24, 25], which is consistent with our microRNA assay data. [score:3]
However, we noticed that unlike the five key miRs we identified neither miR-21 nor miR-181 significantly changed upon SkM treatment post-MI in our study. [score:1]
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[+] score: 4
Other miRNAs from this paper: hsa-mir-16-1, hsa-mir-17, hsa-mir-20a, hsa-mir-21, hsa-mir-23a, hsa-mir-100, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-107, hsa-mir-16-2, mmu-mir-1a-1, mmu-mir-23b, mmu-mir-125b-2, mmu-mir-130a, mmu-mir-9-2, mmu-mir-145a, mmu-mir-181a-2, mmu-mir-184, mmu-mir-199a-1, hsa-mir-199a-1, mmu-mir-205, mmu-mir-206, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-199a-2, hsa-mir-205, hsa-mir-181a-1, hsa-mir-214, hsa-mir-219a-1, hsa-mir-223, mmu-mir-302a, hsa-mir-1-2, hsa-mir-23b, hsa-mir-125b-1, hsa-mir-130a, hsa-mir-145, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125b-2, hsa-mir-184, hsa-mir-206, mmu-mir-16-1, mmu-mir-16-2, mmu-mir-20a, mmu-mir-21a, mmu-mir-23a, mmu-mir-103-1, mmu-mir-103-2, rno-mir-338, mmu-mir-338, rno-mir-20a, hsa-mir-1-1, mmu-mir-1a-2, hsa-mir-181b-2, mmu-mir-107, mmu-mir-17, mmu-mir-100, mmu-mir-181a-1, mmu-mir-214, mmu-mir-219a-1, mmu-mir-223, mmu-mir-199a-2, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-181b-1, mmu-mir-125b-1, hsa-mir-302a, hsa-mir-219a-2, mmu-mir-219a-2, hsa-mir-302b, hsa-mir-302c, hsa-mir-302d, hsa-mir-367, hsa-mir-372, hsa-mir-338, mmu-mir-181b-2, rno-mir-9a-1, rno-mir-9a-3, rno-mir-9a-2, rno-mir-16, rno-mir-17-1, rno-mir-21, rno-mir-23a, rno-mir-23b, rno-mir-100, rno-mir-103-2, rno-mir-103-1, rno-mir-107, rno-mir-125b-1, rno-mir-125b-2, rno-mir-130a, rno-mir-145, rno-mir-181a-2, rno-mir-181b-1, rno-mir-184, rno-mir-199a, rno-mir-205, rno-mir-206, rno-mir-181a-1, rno-mir-214, rno-mir-219a-1, rno-mir-219a-2, rno-mir-223, hsa-mir-512-1, hsa-mir-512-2, rno-mir-1, mmu-mir-367, mmu-mir-302b, mmu-mir-302c, mmu-mir-302d, rno-mir-17-2, hsa-mir-1183, mmu-mir-1b, hsa-mir-302e, hsa-mir-302f, hsa-mir-103b-1, hsa-mir-103b-2, rno-mir-9b-3, rno-mir-9b-1, rno-mir-9b-2, rno-mir-219b, hsa-mir-23c, hsa-mir-219b, mmu-mir-145b, mmu-mir-21b, mmu-mir-21c, mmu-mir-219b, mmu-mir-219c, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
On the other hand, the top upregulated miRNAs at the OP3-OL transition included miRNAs (miR-181a, miR-181b, miR-125b, and miR-184) that are associated with decreased proliferation in maturing CNS cells and decreased malignancy in glioma stem cells [49], [50], [51], [52], [53], [54], [55]. [score:4]
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[+] score: 4
Overall, the expression patterns of miRNAs fell into four main categories: (1) Enriched in early embryonic stages, especially at E10 and E13 and decreased gradually during development (i. e. the rno-miR-181 family); (2) Enriched late postnatally, especially at P14 and P28, and tended to increase over time (i. e. rno-miR-29a and rno-miR-128); (3, 4) Peaked around neonatal stage (P0), either highest peak or lowest peak. [score:4]
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[+] score: 3
org) revealed several miRNA that might interact with POMC mRNA untranslated region, including miR-488, miR-485, miR-384-3p, miR-383, miR-377, miR-485-5p and miR-181 (family). [score:3]
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[+] score: 3
Among these aberrant miRNAs, ten miRs (miR-183-3p, miR-34c-3p, miR-200b, miR-466c, miR-465-3p, miR-185-3p, miR-320a, miR-493-5p, miR-181b-5p and miR-21-5p) were reported to be differentially expressed at both 12 and 48 h after IR. [score:3]
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[+] score: 3
Other miRNAs from this paper: rno-mir-19b-1, rno-mir-19b-2, rno-mir-181b-1, rno-mir-185
For example, miR-181b in serum may be a potential diagnostic biomarker for cirrhosis 24, and miR-19b was found to be up-regulated 4.3-fold in the serum of individuals with cirrhotic livers, compared with normal controls 18. [score:3]
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25
[+] score: 3
The potential miRNA targets of rno_circRNA_008964 included rno-miR-216b-5p, rno-miR-181d-5p, rno-miR-337-5p, rno-miR-497-3p, and rno-miR-181b-5p (Fig. 5a). [score:3]
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[+] score: 3
Moon J. M. Xu L. Giffard R. G. Inhibition of microRNA-181 reduces forebrain ischemia -induced neuronal lossJ. [score:3]
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27
[+] score: 3
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-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
A comparison of effects of ACTH and DEX shows that both hormones increased the expression miRNA-181b, miRNA-672, and miRNA-100, and significantly decreased the levels of miRNA-92a, and miRNA-466b. [score:3]
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[+] score: 3
We found that miRNAs with higher expression in WBCs includes different miRNA families: mir-15, mir-17, mir-181, mir-23, mir-27 and mir-29 families. [score:3]
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29
[+] score: 3
Some of the deregulated miRNAs (miR-181, miR-26, miR-1, mir-29, miR-214, miR-126, and miR-499) are reported to be related to hypoxia, cell development, and cell growth [1, 5, 7, 25]. [score:3]
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30
[+] score: 1
For example, miR-181, miR-124 and let-7d are suggested to be involved in cocaine -induced nervous plasticity and cocaine -induced conditioned place preference (CPP) [7, 8]. [score:1]
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[+] score: 1
The GeNorm algorithm ranked miRNA miR181a-5p and miR181b-5p as the most stable ones and they were used as normalizers to evaluate the relative expression of the remaining miRNA. [score:1]
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[+] score: 1
We found that miR-99, miR-100, miR-208, miR-181, miR-19 and many others were associated to cardiac hypertrophy and apoptosis. [score:1]
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