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61 publications mentioning rno-mir-181a-2

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

[+] score: 178
In summary, we have demonstrated that miR-181a expression is upregulated in H [2]O [2] -treated H9c2 cells and that inhibition of miR-181a confers cardiac protection against oxidative stress -induced H9c2 cell apoptosis through the direct inhibition of Gpx1 expression and ROS generation, which are important for the maintenance of mitochondrial membrane integrity and the inhibition of mitochondrial apoptotic pathway under oxidative stress conditions. [score:15]
We found that miR-181a is upregulated in cardiomyocytes with oxidative stress and that the downregulation of miR-181a significantly inhibited the H [2]O [2] -induced cellular apoptosis, ROS production, mitochondrial structure disruption, and activation of key signaling proteins in the mitochondrial apoptotic pathway. [score:9]
We found that the downregulation of miR-181a expression protected against the H [2]O [2] -induced injury of H9c2 cells by restoring the alterations of H9c2 morphology and nuclear condensation, inhibiting the production of ROS and blocking LDH release and MDA production, two indicators of oxidative stress -induced injury [33]. [score:8]
Therefore, it is reasonable to conclude that miR-181a regulates the expression of Gpx1 and that Gpx1 directly influences the expression of Bcl-2. However, the direct regulation of Bcl-2 by miR-181a has been confirmed by many investigations, mainly in tumor cells [42– 44]. [score:7]
The H [2]O [2 ]treatment increased the generation of cleaved caspase-3. This effect was attenuated by transduction with the anti-miR-181a, whereas the upregulation of miR-181a increased cleaved caspase-3 expression (Figure 6(e)). [score:6]
The transfection with the mature miR-181a resulted in decreased Gpx1 protein expression (* P < 0.01) compared with the control, whereas the anti-miR-181a protected against the mature miR-181a -mediated inhibition of Gpx1 expression (* P < 0.05) (Figure 3(c)). [score:6]
Transduction of the Anti-miR-181a Restored the H [2]O [2]-Altered H9c2 Cell Morphology and Decreased the Levels of LDH and MDAH9c2 cells were transfected as described in Section 2. As shown in Figure 4(a), the mature miR-181a increased miR-181a expression in H9c2 cells, whereas anti-miR-181a decreased miR-181a expression. [score:5]
As expected, Bax expression was markedly decreased by the anti-miR-181a (Figures 6(d) and 6(f)), suggesting that the anti-miR-181a prevents H9c2 cells from undergoing apoptosis by increasing Bcl-2 while inhibiting Bax. [score:5]
To ascertain the role of miR-181a in ROS -mediated H9c2 cells apoptosis, miR-181a expression was modulated via a miR-181a inhibitor and miR-181a mimic. [score:5]
The anti-CTL and anti-miR-181a are represented as the scrambled inhibitor and miR-181a inhibitor, respectively. [score:5]
Furthermore, other studies have demonstrated that miR-181a represses important antiapoptotic targets such as X-linked inhibitor of apoptosis (XIAP), a function that could help explain the proapoptotic effects of this miRNA [32]. [score:5]
H9c2 cells were transfected as described in Section 2. As shown in Figure 4(a), the mature miR-181a increased miR-181a expression in H9c2 cells, whereas anti-miR-181a decreased miR-181a expression. [score:5]
By qPCR analyses, we validated that the miR-181a expression was upregulated approximately 4-fold in H [2]O [2] -treated cells compared with the controls. [score:5]
To further confirm the expression change, a 2 h exposure of H9c2 cells to varying concentrations of H [2]O [2] resulted in concentration -dependent increases in miR-181a expression, with a peak at approximately 400  μM (Figure 2(b)). [score:5]
We demonstrated that the negative effect of miR-181a on the Gpx1 levels in H9c2 cells was the result of the direct targeting of Gpx1 mRNA by miR-181a. [score:4]
At the apoptotic concentration of H [2]O [2], only miR-181a expression was increased compared with the control group, whereas the expression of the other candidate miRNAs was decreased (Figure 2(b)). [score:4]
The effect of H [2]O [2] was attenuated by transduction with the anti-miR-181a, whereas the upregulation of miR-181a exacerbated this effect (Figure 8). [score:4]
In addition, Gpx1 expression in H9c2 cells was regulated by miR-181a in unstimulated cells, as determined both by gain-of-function and loss-of-function approaches. [score:4]
Our results demonstrate that miR-181a regulates the expression of the Bcl-2 family. [score:4]
The miR-181a -mediated suppression was abolished by mutation of the 3′-UTR miR-181a binding site, which disrupts the interaction between miR-181a and the Gpx1-3′-UTR (Figure 3(b)). [score:4]
Prior studies have identified several targets for miR-181a, including GRP78, a major endoplasmic reticulum chaperone and signaling regulator [46, 47], and sirtuin-1, an NAD -dependent protein deacetylase [48]. [score:4]
Downregulation of miR-181a Blocks the Mitochondrial Apoptotic Pathway. [score:4]
The control oligonucleotides had no effect on miR-181a expression. [score:3]
We found that the ratio of the H [2]O [2] group was lower than that of the control group (* P < 0.01), that the anti-miR-181a showed protective effects compared with the anti-CTL -treated groups, and that the upregulation of miR-181a decreased the ratio ([&] P < 0.05, [#] P < 0.05; Figure 7(b)). [score:3]
In the future, luciferase reporter assays and western blot analyses should be used to validate Bcl-2 as a direct target of miR-181a in H9c2 cells. [score:3]
Taken together, these results suggest that miR-181a plays a key role in oxidative stress -induced cardiomyocyte apoptosis and that miR-181a may be linked with the expression of Gpx1. [score:3]
Because Gpx1 catalyzes the reduction of H [2]O [2] to water [5] and miR-181a mediates the suppression of Gpx1 expression, we attempted to investigate the effect of miR-181a upon ROS generation. [score:3]
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]
Quantitative analysis using flow cytometry confirmed that the anti-miR-181a significantly inhibited H [2]O [2] -induced apoptosis (Figures 6(b)- 6(c)). [score:3]
Validation of the In Silico Target Analysis of miR-181a. [score:3]
The H [2]O [2] treatment strikingly increased the MDA level, whereas the miR-181a inhibitor significantly decreased the MDA level (Figure 4(c)). [score:3]
Future studies, especially in ischemia/reperfusion animal mo dels, are necessary to validate the possible therapeutic use of miR-181a regulation. [score:2]
Our study illustrates the role of miR-181a as a proapoptotic modulator in the regulation of Gpx1. [score:2]
Our data demonstrate that the anti-miR-181a blocked H [2]O [2] -induced H9c2 apoptosis by regulating mitochondria-related apoptotic pathways. [score:2]
Predicted miR-181a as a Negative Regulator of Gpx1. [score:2]
H9c2 cells were also transfected with a final concentration of 100 nM and for miR-181a knockdown anti-miR-181a (Guangzhou RiBo Corp. [score:2]
Transduction of the mature miR-181a increased the staining intensity, whereas the anti-miR-181a produced relatively dim DCFH-DA staining. [score:1]
Transduction of the anti-miR-181a, however, nearly restored H9c2 nuclei to the normal morphology (Figure 6(a)). [score:1]
Transduction of the anti-miR-181a, however, almost restored the spindle-shaped morphology observed in untreated cells (Figure 4(b)). [score:1]
HEK293 cells, seeded into 96-well plates at a density of 1.5 × 10 [4] per well, were transfected with pmiR-RB-Gpx1-WT-3′ UTR (100 ng/well), pmiR-RB-Gpx1-Mut-3′ UTR (100 ng/well), mature miR-181a (50 nM), or miR-control (50 nM) using Lipofectamine 2000. [score:1]
Hutchison et al. used microarray analysis to assess the effects of miR-181 on the transcriptome in primary astrocytes. [score:1]
The anti-miR-181a significantly increased Bcl-2 levels while decreasing Bax protein levels, attenuating the alterations caused by H [2]O [2] -induced injury. [score:1]
Transduction of the Anti-miR-181a Restored the H [2]O [2]-Altered H9c2 Cell Morphology and Decreased the Levels of LDH and MDA. [score:1]
Anti-miR-181a Restored the H [2]O [2]-Induced Loss of the Mitochondrial Membrane Potential. [score:1]
These data demonstrate that the anti-miR-181a protected H9c2 cells from H [2]O [2] -induced apoptosis by maintaining mitochondrial membrane integrity and cardiomyocyte function. [score:1]
Transduction of the anti-miR-181a, however, blocked the H [2]O [2] -induced formation of JC-1 monomers (Figure 7(a)), suggesting that the anti-miR-181a can restore the H [2]O [2] -induced loss of the mitochondrial membrane potential. [score:1]
Anti-miR-181a Reduced ROS Production. [score:1]
HEK293 and H9c2 cells were transfected with 50 nM mature miR-181a and miR-CTL (GuangzhouRuiBio Corp. [score:1]
Transduction of the anti-miR-181a, however, restored the mitochondrial membrane potential. [score:1]
Anti-miR-181a Restored the H [2]O [2]-Induced Loss of the Mitochondrial Membrane PotentialUntreated cells contained bright-staining mitochondria that emitted orange fluorescence. [score:1]
The anti-miR-181a contained 2′-OMe modifications at every base. [score:1]
Anti-miR-181a Attenuated H [2]O [2]-Induced H9c2 Cell Apoptosis. [score:1]
These data suggest that the anti-miR-181a attenuates the production of ROS. [score:1]
These data suggest that the anti-miR-181a reduces H [2]O [2] -induced apoptosis by blocking caspase-3 -dependent cardiomyocyte apoptosis. [score:1]
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[+] score: 149
Other miRNAs from this paper: rno-mir-181a-1
Wang et al. studied the target genes of miR-181a in cardiomyocytes and concluded that miR-181a regulated the expression of Gpx1 and that Gpx1 directly influenced the expression of Bcl-2 and played an important role in the regulation of the mitochondrial apoptotic pathway in cardiomyocytes challenged by oxidative stress [9]. [score:10]
Therefore, miR-181a suppressed Bcl-2 expression through the direct targeting of the Bcl-2 transcript in H9c2. [score:8]
To ascertain whether these miR-181a -binding sequences directly contributed to the negative regulation of Bcl-2 expression, we used a luciferase assay to verify that Bcl-2 was the direct target gene that miR-181a regulates H9c2 cells. [score:8]
In addition, we demonstrated that miR-181a suppressed Bcl-2 expression by directly targeting of the Bcl-2 transcript in H9c2 cells (Figure 4(h)). [score:8]
Compared with the iNC + ADM group, the cell viability of myocardial cells transfected with the miRNA-181a inhibitor was significantly increased (P = 0.0427) in miR-181a -inhibitor + ADM group, which indicated that the inhibition of miR-181a in cardiomyocytes attenuated ADM -induced cardiomyocyte death. [score:6]
A significant upregulation of miR-181a expression was found in both ADM-alone group and the combination group (Figures 3(a) and 3(b)). [score:6]
Bcl-2, for which the gene product is known to have a role in apoptosis reduction, was one of the direct target genes of miR-181a [35] and inhibited mitochondrial metabolism and ADM -induced apoptosis in cancer cells [36]. [score:6]
In this study, we found that anthracycline could induce cardiomyocyte apoptosis and upregulated the expression of miR-181a in vitro and in vivo, which revealed that miR-181a was related to anthracycline -induced cell apoptosis. [score:6]
To delineate the underlying mechanism of miR-181a in the protective effect of ADM -induced cardiomyocyte apoptosis, we searched for potential target genes of miR-181a by using several bioinformatics tools, such as TargetScan, miRanda, and PicTar. [score:5]
The qRT-PCR assays showed that the expression of miRNA-181a in H9c2 cells transfected with the miRNA-181a inhibitor plasmid was significantly lower than that of H9c2 cells transfected with a miRNA-181a NC plasmid (P = 0.0015, Figure 4(a)). [score:4]
The site-directed mutagenesis of the miR-181a target site was conducted by using Invitrogen. [score:4]
All these data indicated that propofol could reduce the upregulation of miR-181a induced by ADM. [score:4]
Propofol Reduced the Upregulation of miR-181a by ADM. [score:4]
In contrast, miR-181a was upregulated in patients with AML who had a favorable outcome [31]. [score:4]
Compared with the control cells, the expression of Bcl-2 was significantly increased (P = 0.0007) and the expression of Bax was significantly decreased (P = 0.048) in miR-181a -depleted cells. [score:4]
Some researchers demonstrated that miR-181a regulated the expression of the Bcl-2 family in different cell types [32, 34]. [score:4]
Twenty-four hours prior to transfection, H9c2 cells were plated in 6-well plates (2.5 × 10 [5] cells/well) and then transfected with miR-181a inhibitor (50 nM) or miR negative control (50 nM) by using Lipo2000 (Invitrogen). [score:3]
Rno-miR-181a inhibitor and rno-miR negative control were synthesized by GenePharma (Shanghai). [score:3]
The apoptosis index in rat heart tissue after different treatments was determined by TUNEL staining, and the expression of miR-181a and phospho-STAT3 was determined by RT-qPCR or Western blotting (Figure 5). [score:3]
To confirm the critical role of miR-181a in ADM -induced cardiomyocyte apoptosis in H9c2 cells, we transfected rno-miR-181a inhibitor and rno-miR-181a control into H9c2 cells and detected changes in apoptosis. [score:3]
The upregulation of miR-181a by the combination treatment was reduced compared with ADM alone in H9c2 (P = 0.0048, Figure 3(a)). [score:3]
A low global expression of miR-181a was observed in breast and colon cancer cells [30]. [score:3]
However, this study was the first to confirm the direct regulation between miR-181a and Bcl-2 in rat cardiomyocytes. [score:3]
The differential expression of Bcl-2 and Bax after ADM treatment in miR-181a -depleted cells and control cells was examined by Western blotting (Figure 4(f)). [score:3]
This indicated that anthracycline -induced cardiomyocyte apoptosis and increased the expression of miR-181a and phospho-STAT3 in vivo. [score:3]
Therefore, it was undetermined whether miR-181a functioned as oncogene or tumor suppressor. [score:3]
If miR-181a was capable of binding to the 3′UTR region of the Bcl-2 gene, the luciferase activity decreased in the cells transfected with pGL3-Bcl-2-wt plasmid as the expression of miR-181a increased. [score:3]
To ascertain the role of miR-181a in ADM -induced cardiomyocyte apoptosis, miR-181a expression was tested by RT-PCR. [score:3]
As shown previously, propofol played a protective role in ADM -induced apoptosis, whereas the expression of miR-181a was significantly reduced in the ADM + prop group compared with that in the ADM group. [score:2]
A significant reduction in the expression of miR-181a and phospho-STAT3 occurred in the ADM + prop group compared with that in the ADM-only group, as shown in Figures 5(b) and 5(d) (P < 0.05). [score:2]
Compared with the iNC group (17.2% ± 1.3%), a significant decrease (P = 0.006) in the early apoptosis rate of miR-181a inhibitor cells (12.3% ± 0.9%) was observed (Figures 4(c) and 4(e)). [score:2]
The protective effect may be related to the regulation of the miR-181a/Bcl-2 pathway and the observed negative correlation between miR-181a and Bcl-2 in cardiomyocytes. [score:2]
In future studies, we aim to confirm if propofol regulates cardiomyocyte apoptosis through the STAT3/miR-181a/Bcl-2 pathway and determine the relationship between STAT3 and miR-181a in cardiomyocytes. [score:2]
The importance of miR-181a in cardiomyocyte apoptosis has been confirmed in numerous experiments [8, 9]; however, the role of miR-181a in anthracycline -induced myocardial injury requires further study. [score:1]
The activity of transcription factor STAT3, which orchestrates the induction of miR-181a [32], was lower in the ADM + prop group than in the ADM-alone group (Figures 3(c) and 5(c)), which reflected the significance of miR-181a in the cardioprotective mechanism of propofol. [score:1]
In the present study, the depressed level of miR-181a was mostly restored through the addition of propofol to anthracycline -treated cardiomyocytes in vitro (Figures 2(a) and 2(b)) and in vivo (Figure 5(b)), which indicated that miR-181a was involved in the propofol -mediated relief of doxorubicin -induced cardiomyopathy. [score:1]
As shown in Figure 4(h), luciferase activity was decreased significantly by transfection of the miR-181a mimic when the wild-type 3′UTR of Bcl-2 was present (P = 0.0299), whereas no difference was found after the transfection of the pGL3-Bcl-2-mut vector (P = 0.4611). [score:1]
In this study, we aimed to evaluate the protective effect and mechanism of propofol in the regulation of ANT -induced apoptosis in cardiomyocytes in vitro and in vivo and the role of miR-181a in the regulation of ANT -induced cardiomyocyte apoptosis. [score:1]
The plasmids containing pGL3-Bcl-2-wt or pGL3-Bcl-2-mut and the miR-181a mimic or control mimic were cotransfected. [score:1]
The results of this study revealed that propofol provided cardioprotective effects against ANT -induced cardiotoxicity, which were mediated by miR-181a both in vitro and in vivo. [score:1]
In a recent study by Zhu et al., miR-181a modulated cardiomyocyte apoptosis induced by Necrotic-S -treated dendritic cells (DCs) in hypoxic conditions [8]. [score:1]
The correlation of miR-181a and anthracycline resistance in patients with triple -negative breast cancer was reported by Ouyang et al. [33]. [score:1]
miR-181a, wi dely present in human organs, has been reported to modulate cell proliferation, migration, apoptosis, and tumorigenesis [27– 29]. [score:1]
Propofol Reduced ADM-Induced Apoptosis by miR-181a In Vitro. [score:1]
The computational analysis revealed that there was a binding site on the 3′ UTR of Bcl-2 for miR-181a, which was highly conserved among different species (Figure 4(g)). [score:1]
[1 to 20 of 45 sentences]
[+] score: 81
Analysis of the protein-coding genes differentially expressed in islets of 12-month-old rats revealed significant enrichment for potential targets of miR-181a in the upregulated genes (Fig.   7b, ESM Table 6) and depletion of predicted targets in the downregulated genes (Fig.   7a, ESM Table 7). [score:13]
However, analysis of differentially expressed genes in the islets of 12-month-old rats revealed an enrichment of miR-181a targets in the upregulated mRNAs and a reduction in those that were downregulated. [score:11]
We observed that overexpression of miR-34a (Fig.   6a, b) or downregulation of miR-181a (Fig.   6c, d) did not affect basal beta cell proliferation, but did inhibit proliferation stimulated by exendin-4 or PDGF-AA. [score:8]
The islets of these animals displayed modifications at the level of several miRNAs, including upregulation of miR-34a, miR-124a and miR-383, and downregulation of miR-130b and miR-181a. [score:7]
We indeed confirmed the upregulation of miR-124a and miR-383 and the downregulation of miR-181a and miR-130b observed by microarray (Fig.   2a–d). [score:7]
Downregulation of miR-181a or overexpression of miR-124a modified neither the basal apoptotic rate nor survival in the presence of cytokines (ESM Fig.   5). [score:6]
Computational analysis of the transcriptomic modifications observed in the islets of 12-month-old rats revealed that the differentially expressed genes were enriched for miR-34a and miR-181a targets. [score:5]
Ctrl, control To unravel the mechanisms underlying the effects of miR-34a and miR-181a on age -associated beta cell dysfunction, we searched for potential targets within genes expressed in the islets of aged animals. [score:5]
The median number of recognition elements (M [obs]) for miR-181a (a, b) and miR-34a (c, d) predicted in the 3′ UTR of all down- (a, c) and upregulated (b, d) mRNAs in ageing (arrows) was compared with a null distribution of the median number of predicted recognition elements obtained for 1,000 randomly sampled sets of 3′ UTRs from mRNAs expressed in rat islets. [score:5]
The mechanism through which the downregulation of miR-181a contributes to the age -associated impairment of beta cell proliferation remains to be established. [score:4]
These observations suggest that age -associated changes in miR-181a and miR-34a levels contribute to the gene expression differences observed in the islets of aged rats. [score:3]
Interestingly, overexpression of miR-34a or blockade of miR-181a was sufficient to reproduce this phenotypic trait in the islets of younger animals. [score:3]
Fig. 7Number of miR-34a and miR-181a recognition elements in the 3′ UTR of differentially expressed mRNAs in islets of 12-month-old rats. [score:3]
Indeed, the induction of miR-34a and reduction of miR-181a in the islets of young animals mimicked the impaired beta cell proliferation observed in old animals. [score:1]
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[+] score: 45
Kazenwa del et al. [21] reported that the over -expression of miR-181a in mouse lymphatic endothelial cells directly targeted the 3' UTR of Prox1, and the expression of miR-181a was lower in vascular endothelial cells than in lymphatic endothelial cells. [score:8]
The inhibitory effects of miR-466 on Prox1 expression, tube formation, and lymphatic vessel formation were comparable to those of miR-181. [score:5]
Furthermore, the expression of miR-181a was inversely related to the expression of Prox1 [21]. [score:5]
Another possibility is that miR-181a may also target angiogenesis-related genes other than Prox1 more effectively than miR-466. [score:3]
However, the inhibitory effect of miR-466 on blood vessel formation in the in vivo corneal injury mo del was slightly weaker than that of miR-181a. [score:3]
miR-181a, which is known to target Prox1, was included as a positive control, while a scrambled miRNA was used as a negative control. [score:3]
miR-181a, which was reported to target Prox1, was used as a positive control. [score:3]
Under direct microscopic observation, blood vascular infiltration was about 46% of the scrambled control group level in the miR-181a -treated group. [score:2]
The miR-181a mimic exerted the highest level of inhibitory effects on tube formation (approximately 84%) followed by the miR-466 mimic (approximately 57%; Figure  5B) when compared to the scrambled control. [score:2]
This was considered to be important due to similarity with miR-181a, which was previously shown to target Prox1. [score:2]
Although miR-4262 showed an 8mer seed match with the 3' UTR of Prox1, it was excluded from further study because the 8mer seed sequence of miR-4262 was identical to that of miR-181a. [score:1]
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]
The animals were then randomly allocated to three treatment groups: scrambled control, miR-181a, and miR-466. [score:1]
qRT-PCR revealed that the Prox1 mRNA level was reduced by approximately 50% following transfection with the miR-181a mimic. [score:1]
When the animals were injected with miR-466, corneal thickness was between those observed for the scrambled control and the miR-181a -injected animals, while F-actin positive staining was 56% of the scrambled control group level (Figure  6K). [score:1]
HDLEC were transfected with the miR-181a, miR-466, miR-4305 mimics, or the scrambled control. [score:1]
miR-181a was used as a positive control, while the scrambled miRNA was used as a negative control. [score:1]
In contrast, miR-466- or miR-181a -injected animals showed reduced opacity (Figure  6B and 6C). [score:1]
HDLEC were transfected with miR-181a, miR-466, miR-4305 mimics, or the scrambled control. [score:1]
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[+] score: 44
Overexpression and inhibition of miR-181a can regulate synaptic function by negatively regulating GluA2 expression [25]. [score:9]
The study also found that chronic amphetamine and cocaine treatment could upregulate miR-181a expression in specific brain areas of mice. [score:6]
In contrast, cocaine could significantly upregulate miR-181a in the prefrontal cortex of mice without altering its expression in the hippocampus, nucleus accumbens, or midbrain ventral brain regions, suggesting that different addictive drugs induce miRNAs in different brain regions. [score:6]
The expression of miR-181a in hippocampus, nucleus accumbens, and the midbrain ventral region was upregulated, the most significant change being in hippocampus, while miR-181a in prefrontal cortex showed no significant change. [score:6]
Chandrasekar and Dreyer found that the expression of miR-181a in the nucleus accumbens was upregulated after chronic cocaine administration. [score:6]
In serum exosomes, a total of 962 targets of rno-miR-145-3p, rno-miR-181a-5p, rno-miR-21-5p, rno-miR-200a-5p, rno-miR- 375-3p, and rno-miR-1b were predicted by Target Scan, miRDB, and DIANA Tools. [score:5]
Moreover, activation of dopamine signals in hippocampal neurons can induce miR-181a expression. [score:3]
They also found that miR-181a in cocaine addiction formed a complex regulatory mechanism that impacted neural plasticity and reward circuits [24]. [score:2]
miR-181a-5p is one of the four DE co-miRNAs we found. [score:1]
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[+] score: 36
A recent study showed that miR-181a suppressed the expression of Prox1, which functions as a Notch1 inhibitor, and that up-regulation of Notch1 induced astrocyte differentiation from NPCs [66]. [score:10]
KWV treatment reduced the phosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2), increased mRNA expression levels of the cyclin -dependent kinase inhibitor p21, reduced notch1 and hes1 transcription and up-regulated the miRNAs including miR-9, miR-29a and miR-181a. [score:9]
Assessment of the miRNA expression levels in 2.5 μM of KWV -treated NSCs in the presence of mitogens using RT PCR showed that miR-9, miR-29a, and miR-181a expression were significantly up-regulated (1.44-, 1.51- and 1.34-fold, vs. [score:8]
However, miR-181a overexpression in human dermal fibroblasts resulted in the increase of senescence marker p53 and p16, and subsequent fibroblast senescence [67]. [score:3]
The miScript PCR system (Qiagen) was used to analyze the expression of miRNAs, including rno-miR-9, rno-miR-29a, rno-miR-124 and rno-miR-181a, according to the manufacturer’s instructions. [score:3]
While our results with rat NSCs did not support KWV induction of astrocyte differentiation, KWV treatment did inhibit NSC proliferation, which may be related to the miR-181a increase seen in the NSCs. [score:3]
[1 to 20 of 6 sentences]
[+] score: 34
First, we analyzed the expression levels of the primary transcripts, which demonstrated that both PPT and DPN treatment significantly decreased the expression of pri-miR-7a, pri-miR-125a, pri-miR-181a, and pri-miR-495 compared to either vehicle or E [2] treated animals (Figure 9a). [score:4]
These expression levels decreased with age, whereas an opposite trend was observed in the OVX animals and miR-181a expression was significantly higher in both OVX groups compared to ovarian intact animals by 21 mo. [score:4]
Specifically, E [2] treatment significantly regulated the expression of mature miR-7a, miR-9, miR-9-3p, and miR-181a at 1 week post-OVX, which was consistent with our previously published data, [46], but not at any other time point (Figure 2a–2d, 2f), demonstrating a clear timing effect. [score:4]
Experiment 1: Expression of E [2]-responsive mature miRNAs in the hypothalamus of ovarian intact animals changes with ageOur previous studies showed that E [2] regulated a subset of mature miRNAs (let-7i, miR-7a, miR-9, miR-9–3p, miR-125, miR-181a, and miR-495) in an age- and brain-region dependent manner [46]. [score:4]
These results were unexpected given the E [2] -induced increase in both mature and pri-miR-181a expression levels at varying time points (see Figures 2f and 3h). [score:3]
Further, there was a statistically significant difference in the expression of mature miR-7a, miR-9a-3p, and miR-181a between ovarian intact and OVX+veh treated animals at later time points (i. e. 19, 20, and 21 months). [score:3]
By contrast, PPT significantly increased the expression of the precursor form of miR-181a (pre-miR-181a), but had no effect on the precursor forms for any of the other miRNAs (Figure 9b). [score:3]
miR-181a: Ovarian intact animals had significantly higher levels of miR-181a expression at 18 mo. [score:3]
Our previous studies showed that E [2] regulated a subset of mature miRNAs (let-7i, miR-7a, miR-9, miR-9–3p, miR-125, miR-181a, and miR-495) in an age- and brain-region dependent manner [46]. [score:2]
Finally, E [2] had no effect on pri-miR-181a or pri-miR-495 at any time point (Figure 3h, 3i). [score:1]
One way ANOVA analyses across the deprivation time points showed that pri-mir-7a-2, pri-mir-9-1, pri-mir-125a, pri-mir-181a, and pri-mir-495 were all significantly altered by OVX alone, and in general, they were all decreased with age (Figure 3, black line, #). [score:1]
Interestingly, E [2] completely abolished the steep age-related increase in pre-miR-181a observed at 4 weeks post-OVX (Figure 4f, gray line, *). [score:1]
Further, both primary transcripts for miR-181a and miR-495 were significantly decreased at 4, 8, and 12 weeks post OVX (Figure 3h–3i, black line, #). [score:1]
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[+] score: 33
Interestingly, miR-22, miR-1224 and miR-125-3p were initially up-regulated under EGF and bFGF treatment, but reversed their quantitative expression in the presence of IGF-1. In addition, miR-214 and miR-708 were expressed inconsistently in Group A while their expression went down in Group B. To validate the microRNA microarray expression data, a qRT-PCR assay was conducted to confirm the expression levels of three randomly selected microRNAs (let 7-b, miR-181a, and miR26a). [score:13]
The expression of let-7b was down-regulated on both Day 3 (Figure 3C) and Day 5 (Figure 3D) after induction whereas miR-181a and miR-26a remained up-regulated. [score:9]
Of these, let-7b was from the down-regulated list, and miR-26a and miR-181a were from the up-regulated list. [score:7]
The qRT-PCR analysis confirmed that let-7b, miR-181a, and miR-26a were significantly up-regulated on Day 1 after differentiation (Figure 3B). [score:4]
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[+] score: 26
Among the 11 significantly dysregulated miRNAs, 4 miRNAs were up-regulated (miR-34c, miR-374, miR-181a, and miR-let-7c-1), and 7 miRNAs were down-regulated (miR-1188, miR-770-5p, miR-127-5p, miR-375, miR-331, miR-873-5p, and miR-328a) (differentially expressed miRNAs were defined by a fold-change >1.5, up or down-regulated; p <0.05). [score:13]
Some of the up-regulated (miR-34c, miR-374, miR-181a, and miR-let-7c-1) and down-regulated (miR-1188, miR-770-5p, miR-127-5p, miR-375, miR-331, miR-873-5p, and miR-328a) miRNAs we detected using miRNA microarray were suggested to be closely connected with memory function. [score:7]
Inhibiting miR-181a was proved to be correlated with the protection of 10 μmol/L propofol against GD stress in astrocytes by up -regulating Bcl-2 protein expression[47]. [score:6]
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[+] score: 24
They found that chronic cocaine administration suppressed the expression of miR-124 and let-7d, but induced miR-181a in the mesolimbic dopaminergic system. [score:5]
Regulation of MiR-124, Let-7d, and MiR-181a in the accumbens affects the expression, extinction, and reinstatement of cocaine -induced conditioned place preference. [score:3]
Chandrasekar and Dreyer identified another set of miRNAs (miR-181a, let-7d, and miR-124) whose expression is sensitive to cocaine (Chandrasekar and Dreyer, 2009). [score:3]
In a recent study by Saba et al. it was found that miR-181a expression in nucleus accumbens was increased by dopamine -mediated transmission and by the psychomotor stimulant drugs cocaine and amphetamines (Saba et al., 2012). [score:3]
Dopamine-regulated microRNA MiR-181a controls GluA2 surface expression in hippocampal neurons. [score:3]
Moreover, miR-181a was shown to repress GluA2-AMPA receptor subunit expression, and thereby modulate the magnitude of AMPA receptor clustering. [score:3]
Hence, miR-181a may be a key miRNA involved in drug -induced remo deling of the nucleus accumbens and greater striatal complex in response to drug exposure, thereby driving regulating the emergence of addiction. [score:2]
microRNAs miR-124, let-7d and miR-181a regulate cocaine -induced plasticity. [score:2]
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[+] score: 24
miR-22 plays a critical role in the regulation of cellular proliferation, differentiation, and stress -induced hypertrophy miR-181a MAPK1, TNFα, GATA4 The expression of miR-181a was downregulated during physiological hypertrophy. [score:7]
Since there is no inflammatory response during physiological hypertrophy, expression of miR-181a was identified as downregulated (Fig. 2). [score:6]
miR-99b, miR-100, miR-191a, miR-22 and miR-181a were significantly downregulated during hypertrophy (Fig. 2B). [score:4]
miR-181a expression was induced during inflammation. [score:3]
miR-181a protects the system from injury caused by inflammation by interfering the NF-κB functioning [26] and cell proliferation. [score:1]
miR-181a was reported to play a vital role during inflammatory response in cardiovascular system. [score:1]
miR-181a protects the system from inflammation injury by interfering the NF- κB functioning [26] and cell proliferation. [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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[+] score: 24
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]
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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[+] score: 23
A) Expression level of miR-181a precursor, miR-181a-2, on the mRNA Exon array, B) expression level of mature miR-181a transcript on the miRNA array, C) expression level of mature miR-212 transcript miR-212 on the miRNA array. [score:7]
Upregulation of miR-181a following amphetamine exposure has been reported in the ventral midbrain [17], consistent with our observation of increased expression of the precursor transcript on methamphetamine self-administration. [score:6]
We observed upregulation of the precursor transcript miR-181a-2 on the Exon array (fold change (log2) = −0.69, adj p = 0.00085). [score:4]
We identified 78 miRNA and 150 mRNA transcripts that were differentially expressed (fdr adjusted p < 0.05, absolute log2 fold change >0.5); these included genes not previously associated with addiction (miR-125a-5p, miR-145 and Foxa1), loci encoding receptors related to drug addiction behaviors and genes with previously recognized roles in addiction such as miR-124, miR-181a, DAT and Ret. [score:3]
Boxplots showing expression levels of miR-181a and miR-212 on the arrays. [score:3]
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[+] score: 21
More importantly, the miRNAs analyzed in this study not only included the miRNAs like Let-7a, miR-15b, miR24, miR-100 and miR-125 which may suppress the expression of cyclins A and B, and miRNAs such as Let-7a, miR24 and miR-125 which may regulate activity of CDK1, but also miRNAs such as miR-181a, miR-221 and miR-222 which can target CDK inhibitors [30– 32]. [score:10]
To investigate whether miRNAs have a role in the cell cycle regulation of splenocytes following aniline exposure, the expression of miRNAs, including Let-7a, miR-15b, miR24, miR-100, miR-125, miR-181a, miR-221 and miR-222 which are known to mainly control G2/M phase regulators [30– 32], was analyzed by using real-time PCR and the results are presented in Fig 7. Aniline exposure led to significantly decreased expression of Let-7a (decreased 82%), miR-15b (decreased 62%), miR24 (decreased 78%), miR-100 (decreased 63%), miR-125 (decreased 86%), whereas miR-181a, miR-221 and miR-222 increased by 155%, 78% and 56%, respectively, in comparison to controls (Fig 7). [score:5]
Therefore, greater decreases in Let-7a, miR-15b, miR24, miR-100 and miR-125 expression and significant increases in miR-181a, miR-221 and miR-222 levels in the spleens following aniline treatment may be mechanistically important in generalizing that aniline exposure leads to increased cyclin A, cyclin B, CDK1, and decreased p21, p27, thus triggering the splenocytes to go through G2/M transition. [score:3]
Real-time PCR analysis of miRNAs Let-7a, miR-15b, miR24, miR-100 and miR-125 (A), and miRNAs miR-181a, miR-221 and miR-222 (B) expression in rat spleens following aniline exposure. [score:3]
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[+] score: 20
We also found that miR-659-3p but not miR-181a-5p overexpression led to a significant decrease in luciferase expression from the pGLO- GRN-3′UTR reporter compared to cells transfected with psiUx-empty (Figures 2C,D). [score:4]
To further validate the effect of miR-659-3p on the expression of the endogenous PGRN, HeLa cells were transfected with either psiUx-miR-659 or psiUx-miR-181a. [score:3]
A plasmid overexpressing miR-181a (psiUx-miR-181a) was used as a negative control since no binding site for miR-181a-5p was predicted on GRN 3′UTR. [score:3]
GRN 3′UTR was cloned downstream of the firefly luciferase gene in pGLO vector and co -transfected with 435 ng of miR-659 and miR-181a -overexpressing plasmids in HeLa cells. [score:3]
Fifteen nanograms of GRN 3′-UTR3′UTR cloned downstream of the firefly luciferase gene in pGLO vector was co -transfected with increasing amounts of miR-659 and miR-181a -overexpressing plasmids. [score:3]
Based on these results, we chose to transfect 435 ng of miRNA -overexpressing plasmid and we observed that miR-659-3p overexpression induced a reduction of luciferase activity at 24 h (Figure 2C) and 48 h (Figure 2D), compared to the luciferase activity measured in the same cells transfected with miR-181a-overespressing plasmid. [score:2]
The levels of miR-181a-5p, already present in HeLa cells, were also increased at 24 h and 48 h albeit by smaller amounts. [score:1]
We found a significant effect with 435 ng and 535 ng of psiUx-miR-659 with respect to psiUx-miR-181a Supplementary Figure S1. [score:1]
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[+] score: 18
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]
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]
MiR-181a and miR-181b of the miR-181 family are tumor suppressors for inducing apoptosis [57]. [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]
MiR-181 induced apoptosis in astrocytes by targeting multiple members of the Bcl-2 family [58]. [score:2]
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]
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[+] score: 16
Although the direction of these and the placental miR-181a changes are opposed to the downregulation found in human preterm birth [32], their differential expression across generations coincides with shortened gestational length and indicates a causal or, at least, predictive signature of preterm birth. [score:7]
In the F2-SNN and F2-SSS groups, however, miR-181a was significantly upregulated compared to F2-NNN animals (n = 3, P <0.001 and P <0.01, respectively; Figure  5C), indicating programming by the cumulative effects of stress. [score:3]
Ancestral stress elevated miR-181a expression in female offspring in the F2 generation, but not in F1 animals. [score:3]
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]
Additionally, stress increased placental miR-181a, a marker of human PTB. [score:1]
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[+] score: 13
These selected miRNAs included the seven most strongly upregulated miRNAs (miR-330, miR-338, miR-223, miR-20a, miR-181a, miR-592, miR-212) in the Ago2 IP at 30 min, the only downregulated miRNA (miR-29b) in the Ago2 IP at 30 min, and the three most strongly upregulated miRNAs (miR-219, miR-384, let-7f) in the Ago2 IP at 120 min post-HFS (significant by t-test with Dunn–Bonferroni correction and 1-Way ANOVA with LSD test). [score:10]
miR-181a levels were detected in the HFS -treated dentate gyrus but were below the detection limit in the contralateral (unstimulated) dentate gyrus. [score:1]
miR-181a was therefore excluded from quantitative analysis. [score:1]
Two miRNAs (miR-181a and miR-193a) were undetectable in the control dentate gyrus because their Ct values were greater than 40, and were therefore excluded from the analyses. [score:1]
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[+] score: 12
Age-specific changes in miRNA expression were found for miR-296*, miR-196a (Figure  5H-I), miR-181a, miR-214, miR-363, and miR-18a (Figure  6D-G) which showed high expression at 2 weeks of age in both sexes, followed by low and decreasing expression at all subsequent ages. [score:7]
MiRNAs associated with young age expression showed the highest enrichment for pathways involved in renal inflammation/nephritis (miR-130b, miR-363, miR-296*) and cancer (miR-214, miR-130b, miR-18a, miR-181a, miR-363, miR-196a). [score:3]
More than 15 cancer-related pathways ranked among the top findings for the young age group and included common miRNAs: miR-363, miR-181a, miR-130b, and miR-18a (Figures  5 and 6). [score:1]
MiR-181a and miR-130b have also been shown to be involved in endothelial cell proliferation [43]. [score:1]
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[+] score: 11
MiR-181a is reported to control osteopontin expression in cancer cell and inhibit expression in bone marrow-derived mesenchymal stem cells to maintain bone remo deling balance [44, 45]. [score:6]
The level of expressed miRNAs of interest, rno-miR-199a-3p, rno-miR-181a-5p, rno-miR-140-3p and rno-miR-27b-3p, were confirmed by quantitative RT-PCR in articular cartilage and subchondral bone (Figure 5A and 5B). [score:3]
The rno-miR-199a-3p, rno-miR-181a-5p, rno-miR-140-3p and rno-miR-27b-3p were measured from articular cartilage A. and subchondral bone B. The expression profiles of each miRNA matched the tested probes at least three times repeat. [score:1]
Figure 5The rno-miR-199a-3p, rno-miR-181a-5p, rno-miR-140-3p and rno-miR-27b-3p were measured from articular cartilage A. and subchondral bone B. The expression profiles of each miRNA matched the tested probes at least three times repeat. [score:1]
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[+] score: 11
In addition, immune cell infiltration might be related to the down-regulation of miR-181a expression [23]. [score:6]
For instance, the overexpression and knockdown of miR-181a in primary neurons revealed the effectiveness of miR-181a in the regulation of the GluR2 subunit of the AMPA receptor [57], a key factor in synaptic plasticity. [score:5]
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[+] score: 9
rno-miR-184, rno-miR-347, rno-miR-181a-2-3p, rno-miR-204-5p, rno-miR-132-3p and rno-miR-328b-3p are significantly up-regulated while other 10 miRNAs are significantly down-regulated Fig. 16 Hierarchical clusterings analysis of miRNA expressionprofile for intrauterine infection group and control at P3. [score:9]
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[+] score: 9
It has previously been reported that upregulating miR-21 or downregulating miR-181a reduces H [2]O [2] -induced apoptosis in H9C2 cardiomyocytes, and that overexpressing miR-210 contributes to the protective effect of insulin against apoptosis in H [2]O [2] -treated H9C2 cardiomyocytes [34– 36]. [score:9]
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[+] score: 8
MiR-148-3p, mir-17-5p, miR-181a-5p, miR-19b-3p and miR-24-3p were predicted to control the expression of the following target genes: Interleukin 6 signal transducer IL6ST (gp130). [score:5]
Amongst the 5 miRNAs (miR148-3p, miR17-5p, miR181a-5p, miR19b-3p and miR24-3p) targeting multiple genes from our 70 genes list, mir17-5p, which is increased with stress was confirmed by qRT-PCR. [score:3]
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[+] score: 8
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-181b-1, rno-mir-181b-2, rno-mir-194-1, rno-mir-194-2, rno-mir-208a, rno-mir-181a-1, hsa-mir-423, hsa-mir-18b, hsa-mir-20b, hsa-mir-451a, mmu-mir-451a, rno-mir-451, ssc-mir-122, ssc-mir-15b, ssc-mir-181b-2, ssc-mir-19a, ssc-mir-20a, ssc-mir-26a, ssc-mir-326, ssc-mir-181c, ssc-let-7c, ssc-let-7f-1, ssc-let-7i, ssc-mir-18a, ssc-mir-29c, ssc-mir-30c-2, hsa-mir-484, hsa-mir-181d, hsa-mir-499a, rno-mir-1, rno-mir-133b, mmu-mir-484, mmu-mir-20b, rno-mir-20b, rno-mir-378a, rno-mir-499, hsa-mir-378d-2, mmu-mir-423, mmu-mir-499, mmu-mir-181d, mmu-mir-18b, mmu-mir-208b, hsa-mir-208b, rno-mir-17-2, rno-mir-181d, rno-mir-423, rno-mir-484, mmu-mir-1b, ssc-mir-15a, ssc-mir-16-2, ssc-mir-16-1, ssc-mir-17, ssc-mir-130a, ssc-mir-101-1, ssc-mir-101-2, ssc-mir-133a-1, ssc-mir-1, ssc-mir-181a-1, ssc-let-7a-1, ssc-let-7e, ssc-let-7g, ssc-mir-378-1, ssc-mir-133b, ssc-mir-499, ssc-mir-143, ssc-mir-423, ssc-mir-181a-2, ssc-mir-181b-1, ssc-mir-181d, ssc-mir-98, ssc-mir-208b, ssc-mir-142, ssc-mir-19b-1, hsa-mir-378b, ssc-mir-22, rno-mir-126b, rno-mir-208b, rno-mir-133c, hsa-mir-378c, ssc-mir-194b, ssc-mir-133a-2, ssc-mir-484, ssc-mir-30c-1, ssc-mir-126, ssc-mir-378-2, ssc-mir-451, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, mmu-mir-378b, mmu-mir-101c, hsa-mir-451b, hsa-mir-499b, ssc-let-7a-2, ssc-mir-18b, hsa-mir-378j, rno-mir-378b, mmu-mir-133c, mmu-let-7j, mmu-mir-378c, mmu-mir-378d, mmu-mir-451b, ssc-let-7d, ssc-let-7f-2, ssc-mir-20b-1, ssc-mir-20b-2, ssc-mir-194a, mmu-let-7k, mmu-mir-126b, mmu-mir-142b, rno-let-7g, rno-mir-15a, ssc-mir-378b, rno-mir-29c-2, rno-mir-1b, ssc-mir-26b
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]
Additionally, miR-1 and miR-133 in the heart, miR-181a and miR-142-3p in the thymus, miR-194 in the liver, and miR-143 in the stomach showed the highest levels of expression. [score:3]
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[+] 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
Conversely, miR-181a-5p expression levels in Ad-GFP transduced B13 cells were unchanged compared to non-transduced B13 cells (Fig 6F). [score:2]
0145116.g006 Fig 6Relative miRNA expression levels of miR-200c-3p (A), miR-141-3p (B), miR-325-3p (C), miR-2137 (D), miR-210-3p (E), miR-181a-5p (F), miR-204-5p (G), miR-455-3p (H), miR-137-3p (I), miR-135a-5p (J), miR-384-5p (K) in rat exocrine fractions, rat islets, AR42J cells, B13 cells and B13 transduced with Ad-GFP or Ad-PNM at 4 days post-transduction, quantified by individual qPCR assays. [score:2]
Relative miRNA expression levels of miR-200c-3p (A), miR-141-3p (B), miR-325-3p (C), miR-2137 (D), miR-210-3p (E), miR-181a-5p (F), miR-204-5p (G), miR-455-3p (H), miR-137-3p (I), miR-135a-5p (J), miR-384-5p (K) in rat exocrine fractions, rat islets, AR42J cells, B13 cells and B13 transduced with Ad-GFP or Ad-PNM at 4 days post-transduction, quantified by individual qPCR assays. [score:2]
9 miRNAs were present in two categories; 5 of them were common between Tables 1 and 2 (miR-181a-5p, miR-204-5p and miR-2137, miR-421-3p and miR-483-3p), two miRNAs were present in both Tables 2 and 3 (miR-148a-5p and piR-335-3p) and the remaining two miRNAs were classified both in Tables 1 and 3 (miR-137-3p and miR-455-3p). [score:1]
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[+] 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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[+] score: 7
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]
The expression patterns of some miRNAs observed in our study are consistent with what were observed in previous studies by using the blot-array and Northern blot assays, i. e. miR-125b, miR-9, and miR-181a [6], as well as miR-29a, miR-138 and miR-92 [53]. [score:2]
In contrast, several E10-enriched miRNAs identified in our study, including rno-miR-181a, rno-miR-449a, and rno-miR-503, were not detected in their results. [score:1]
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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-181b-1, rno-mir-181b-2, 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
Additionally, another evidence collected from the current inverstigation demonstrate that the microRNA -mediated regulation is not limited to the 3’UTR, the functionality of target sites in the CDS also confirmed by previous studies [57– 59], such as miR-24 [58], miR-296, miR-470, miR-134 [60], miR-126 [43], miR-181a [59], miR-148 [57] and miR-519 [61] that target sequences within the mRNA coding region have been reported to repress the biosynthesis of the encoded proteins in similar way. [score:6]
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[+] score: 6
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]
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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[+] score: 6
Besides, miR-140, miR-181a-5p and miR-451 expression were all highly increased during fracture healing process [18] and miR-21 overexpression [19] or miR-92a knockdown [20] would enhance fracture healing property. [score:6]
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[+] score: 5
MiRNA-181a which plays a critical role in the inflammatory response and development of immune system [45] was found to be also upregulated in the activated astrocytes. [score:4]
Reduction of miRNA-181a levels is associated with reduced cell death, reduced oxidative stress, and preserved mitochondrial function in astrocytes [46]. [score:1]
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[+] score: 5
Among the moderately up-regulated miRNAs, miR-451 and miR-181a have been well studied. [score:4]
In addition, miR-181a has been demonstrated to be responsible for the genesis of human liver cancer stem/progenitor cells [55]. [score:1]
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[+] score: 5
Zhu et al. [31] reported that the CDDP -induced apoptosis of tubular epithelial cells was modulated by the suppression of Bcl-2 expression by miR-181a. [score:5]
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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-181b-1, rno-mir-181b-2, 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
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-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-182, 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
-673, miR-692, and miR-879) and 4 were downregulated (miR-106a, miR-181a, miR-369, and miR-669k). [score:4]
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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
In agreement with their results, we observed the downregulation of miR-127, miR-181a, miR-411, miR-99a, miR-34a, miR-30b, and miR-30c, which according to Liu [6] should lead to increased inflammation. [score:4]
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[+] score: 4
Furthermore, among these miRNAs, many were found to be involved in angiogenesis, including several with a regulatory function in cell proliferation, the expression of growth factors and extracellular proteolysis, such as miR-497, miR-98, miR-181a, miR-145, miR-29b and miR-27a 24– 29. [score:4]
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[+] score: 4
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-181b-1, rno-mir-181b-2, rno-mir-184, rno-mir-199a, rno-mir-205, rno-mir-206, rno-mir-181a-1, rno-mir-214, rno-mir-219a-1, rno-mir-219a-2, rno-mir-223, hsa-mir-512-1, hsa-mir-512-2, rno-mir-1, mmu-mir-367, mmu-mir-302b, mmu-mir-302c, mmu-mir-302d, rno-mir-17-2, hsa-mir-1183, mmu-mir-1b, hsa-mir-302e, hsa-mir-302f, hsa-mir-103b-1, hsa-mir-103b-2, rno-mir-9b-3, rno-mir-9b-1, rno-mir-9b-2, rno-mir-219b, hsa-mir-23c, hsa-mir-219b, mmu-mir-145b, mmu-mir-21b, mmu-mir-21c, mmu-mir-219b, mmu-mir-219c, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
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
A recent report also showed that another member of the miR-181c family, miR-181a, could influence cerebral ischemia outcomes in vitro and in vivo by regulating GRP78 expression in astrocytes [40]. [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
Other miRNAs from this paper: rno-mir-16, rno-mir-181a-1
Daily variations in the expression of miR-16 and miR-181a in human leukocytes. [score:3]
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[+] 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]
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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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[+] score: 3
Other miRNAs have been implicated in various kidney diseases, including in renal fibrosis (miR-22) [49], nephritic syndrome (miR-181a) [50], and renal cell carcinoma (miR-378) [51]. [score:3]
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[+] score: 3
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]
Ten miRNAs, miR-20b, miR-145, miR-152, miR-155, miR-181a, miR-203, miR-222, miR-301a, miR-324-5p, and miR-351. [score:1]
Similar analysis of “late” group, including c-Maf, Ets1, N-Myc, Nfat5, and Nfib, yielded 10 miRNAs: miR-20b, miR-145, miR-152, miR-155, miR-181a, miR-203, miR-222, miR-301a, miR-324-5p, and miR-351, with multiple connections. [score:1]
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[+] score: 3
Among miRNAs that were present at higher levels in colostrum whey, let-7i, miR-148b-3p, miR-27b, and miR-125b-3p affect the function of antigen-presenting cells, and miR-15b, miR-24, miR-92a, miR-181a, miR-181c, and miR-181d affect T cell development and function [29], [30], [35]. [score:2]
On the other hand, other miRNAs such as, let-7i, miR-143, miR-148b-3p, miR-15b, miR-17-5p, miR-24, miR-27b, miR-92a, miR-106b, miR-125b-5p, miR-181a, miR-181c, miR-181d, miR-200c, miR-375, miR-107, miR-141, and miR-370, were present at higher levels in colostrum whey than in mature milk whey (Fig. 6). [score:1]
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[+] score: 3
We found that miRNAs with higher expression in WBCs includes different miRNA families: mir-15, mir-17, mir-181, mir-23, mir-27 and mir-29 families. [score:3]
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[+] score: 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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[+] score: 3
Chen G. Shen Z. -L. Wang L. Lv C. -Y. Huang X. -E. Zhou R. -P. Hsa-miR-181a-5p expression and effects on cell proliferation in gastric cancerAsian Pac. [score:3]
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[+] score: 2
Recently, some miRNAs in the nucleus accumbens have been reported to be involved in behavioral changes in cocaine CPP, such as miR-181a, miR-124 and let-7b [7, 8]. [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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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]
The GeNorm algorithm ranked miR23a-3p, miR146a-5p and miR181a-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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Normalization was performed to miR-103a-3p, miR-107, miR-181a-3p, miR-181a-5p, miR24-3p, miR-451a, let-7i-5p, and miR23-3p. [score:1]
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Reference miRNAs (rno-miR-27b-3p, rno-miR-21-5p, rno-miR-151-3p, rno-miR-191a-5p, mmu-miR-351-5p, rno-miR-125a-5p, rno-miR-181a-5p) were selected using geNorm [6], and reached stability criteria. [score:1]
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To validate the accuracy and reliability of the microarray profiling data, some transcripts, including four circRNAs (rno_circRNA_001555, rno_circRNA_010684, rno_circRNA_01398, and rno_circRNA_017759), four miRNAs (rno-miR-181a-2-3p, rno-miR-124-3p, rno-miR-136-3p, and rno-miR-206-3p), and four mRNAs (IGF2, IGFBP2, S100a8, and IGF1) were randomly selected for quantitative real-time polymerase chain reaction (qRT-PCR) analysis in nine samples including those used for microarray analysis. [score:1]
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For example, while the exact mature sequence of miR-22 constituted 93.04±0.35% of its total reads, the exact mature sequence of miR-181a only constituted 51.09±0.59%. [score:1]
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miR-181a-5p. [score:1]
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Other miRNAs from this paper: rno-mir-34a, rno-mir-146a, rno-mir-181a-1
MitomiRs in human inflamm-aging: a hypothesis involving miR-181a, miR-34a and miR-146a. [score:1]
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