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36 publications mentioning rno-mir-181c

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

1
[+] score: 211
Wefound that OGD downregulated miR-181c expression but upregulated TNF-α expression. [score:11]
OGD also downregulated miR-181c expression and upregulated TNF-α expression. [score:11]
Further studies showed that miR-181c could directly target the 3′-untranslated region of TNF-α mRNA, suppressing its mRNA and protein expression. [score:10]
By contrast, the ectopic expression of TNF-α using a TNF-α expression vector that encoded the entire coding sequence of TNF but lacked its 3′-UTR expression significantly abrogated miR-181c -induced neuronal survival (Figure 5E,F), indicating that TNF-α is a functional target for miR-181c. [score:9]
Coexpression of miR-181c significantly suppressed the firefly luciferase reporter activity of the wild-type 3′-UTR but not of the mutant 3′-UTR in both HEK193T (Figure 3B) and BV-2 cells (Figure 3C), indicating that miR-181c suppresses TNF-α expression through miRNA binding sequences in its 3′-UTR. [score:9]
As detailed above, OGD upregulated TNF-α and downregulated miR-181c expression in microglial cells. [score:9]
Taken together, this result suggests that miR-181c suppresses TNF-α expression by binding to the 3′-UTR, and that TNF-α is a direct target of miR-181c. [score:8]
In our study, we found that OGD resulted in increased production of NO, whereas ectopic expression of miR-181c could suppress expression of iNOS, leading to decreased production of NO. [score:7]
Downregulation of miR-181c leads to increased TNF-α production, as TNF-α is a direct target of miR-181c. [score:7]
To better understand this regulatory relationship, the capacity of miR-181c to directly regulate TNF-α expression by binding to its 3′-UTR was confirmed. [score:6]
RNAinterference -mediated knockdown of TNF-α phenocopied the effect of miR-181c -mediated neuronal protection, whereas overexpression of TNF-α blocked the miR-181c -dependent suppression of apoptosis. [score:6]
We analyzed the predicted TNF-α -regulating miRNAs that were downregulated in activated microglial cells, and found that TNF-α might be regulated by miR-181c. [score:6]
The ectopic expression of miR-181c significantly reduced the neuronal apoptosis induced by OGD-activated microglia (Figure 4C,D), suggesting that ectopic expression of miR-181c attenuates OGD-activated BV2 -induced neuronal apoptosis. [score:5]
TNF-α exhibited increased levels of mRNA expression, whereas expression of miR-181c was significantly decreased after treatment (Figure 2C). [score:5]
As seenwith the BV-2 cells, miR-181c transfection significantly suppressed basal TNF-α mRNA and protein expression levels (Figure 6A,B). [score:5]
Finally, as seen with the BV-2 cells, we found that miR-181c inhibited OGD -induced iNOS expression and NO production in primary rat microglia (Figure 6E,F). [score:5]
To confirm whether the ectopic miR-181c expression was able to attenuate activated microglia -induced neuronal death, neurons were exposed to cell-free conditioned medium collected from microglia with or without the ectopic expression of miR-181c. [score:5]
miR-181c was capable of significantly suppressing the mRNA and protein expression of TNF-α (Figure 3D). [score:5]
To determine whether the dysregulated miRNAs were functional, we confirmed that ectopic expression of miR-181c resulted in decreased release of TNF-α from the microglial cells and decreased neuronal apoptosis. [score:4]
We hypothesized that increased TNF-α production might result from the downregulation of miR-181c. [score:4]
Hypoxia-ischemia resulted in microglia activation and miR-181c downregulation. [score:4]
miR-181c exhibited the highest degree of downregulation in the activated microglia (Figure 2A). [score:4]
Our data suggest a potential role for miR-181c in the regulation of TNF-α expression after ischemia/hypoxia and microglia -mediated neuronal injury. [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]
Therefore, our data suggest an important role for miR-181c in the regulation of TNF-α expression after ischemia/hypoxia and microglia -mediated neuronal injury. [score:4]
These results confirmed an inverse correlation between expression of miR-181c and TNF-α during hypoxia -induced microglial activation. [score:3]
In addition, the miR-181c -transfected cells exhibited decreased iNOS expression and NO production (Figure 4B). [score:3]
This system was also used to confirm that ectopic expression of miR-181c-attenuated neuronal death was caused by activated primary rat microglia (Figure 6D). [score:3]
In addition, for the first time, we have also identified in microglia a microRNA, miR-181c, whichcan directly regulate TNF-α production post-transcription. [score:3]
Additionally, ectopic TNF-α expression significantly abrogated the neuronal survivalinducec by miR-181c. [score:3]
To confirm this inverse correlation between the expression of miR-181c and TNF-α found in this study, we measured the mRNA expression levels of TNF-α at different time points after OGD treatment. [score:3]
To generate the miR-181c expression vector, the miR-181c gene was amplified from mouse genomic DNA and cloned into the pcDNA3.0 vector (Invitrogen Corp. [score:3]
In addition, a luciferase reporter assay was conducted to confirm whether TNF-α is a direct target of miR-181c. [score:3]
The overproduction of TNF-α that followed OGD -induced microglial activation induced neuronal apoptosis, whereas ectopic expression of miR-181c partially protected neurons from cell death caused by OGD-activated microglia. [score:3]
Overproduction of TNF-α after OGD -induced microglial activation provoked neuronal apoptosis, whereas the ectopic expression of miR-181c partially protected neurons from cell death caused by OGD-activated microglia. [score:3]
Taken together, the results indicate that miR-181c controls microglia -mediated neuronal apoptosis by suppressing TNF-α production (Figure 7). [score:3]
In addition, OGD led to overproduction of secreted TNF-α in the primary rat microglia, whereas ectopic expression of miR-181c significantly reduced TNF-α production (Figure 6C). [score:3]
Mutations were generated in the TNF-α 3′-UTR sequences complementary to the seed region of miR-181c, as indicated. [score:2]
NC represents the negative control for the miR-181c mimics. [score:1]
The miRNA duplexes corresponding to miR-181c were designed as described previously [27]. [score:1]
NC represents thenegative control for the miR-181c mimics. [score:1]
Therefore, our study indicates an important role of miR-181c in TNF-α -mediated neurotoxicity after ischemia (Figure 7). [score:1]
Furthermore, addition of sTNF-α significantly abrogated miR-181c -mediated neuronal survival (Figure 5B). [score:1]
The luciferase activity of the NC transfection in each experiment was used to normalize the data; the luciferase activity of the NC transfection was set to 1. (D) BV-2 cells were transfected with miR-181c mimics or NC. [score:1]
Therefore, we transfected microglial cells with NC or miR-181c mimics and treated the microglial cells with OGD. [score:1]
Ctrl represents the microglial cells that were not treated with oligonucleotide transfection; NC represents the negative control for the miR-181c mimics. [score:1]
Silencing TNF-α also produced a significant decrease in neuronal apoptosis in microglia-conditioned media, which was similar to the phenotype induced by miR-181c. [score:1]
Ctrl represents the control microglial cells that were not subjected to OGD treatment; NC represents the negative control for the miR-181c mimics. [score:1]
Finally, BV-2 cells were transfected with the NC or miR-181c duplexes. [score:1]
We found that silencing of TNF-α in the microglia-conditioned media significantly decreased both TNF-α production (Figure 5C) and microglia -mediated neuronal apoptosis (Figure 5D), which was similar to the phenotype induced by miR-181c. [score:1]
To clarify the role of microglia-derived TNF-α in miR-181c -mediated neuronal apoptosis, we first tested the capacity of TNF-α to trigger death in cultured neurons. [score:1]
Figure 6. (A- B) Primary rat microglia cells were transfected with miR-181c mimics or NC. [score:1]
uk) sitesshowed that TNF-α mRNAs have conserved miR-181c recognition sites in their 3′-UTRs (Figure 2B). [score:1]
Figure 4. (A- B) BV-2 cells were transfected with miR-181c mimics or NC 24 hoursbefore activation by OGD. [score:1]
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2
[+] score: 163
Indeed, we found a significant decrease of both mRNA (Fig. 5A) and total protein content (Fig. 5B) of mt-COX1 in the miR-181c overexpressing hearts, confirming our in-vitro observation that miR-181c regulates mt-COX1 expression [5]. [score:6]
In this study we have shown that chronic overexpression of miR-181c in the rat heart leads to significant down-regulation of mt-COX1 and mt-COX2 (Fig. 5A–B). [score:6]
Taken together, the results demonstrate that chronic overexpression of miR-181c has a role in heart failure by targeting the mitochondrial gene, mt-COX1, which ultimately leads to dysfunctional complex IV, altered mitochondrial metabolism, and ROS generation. [score:5]
Content of mRNA was first normalized to 12S rRNA, a mitochondrial gene, as 12S rRNA expression did not change with miR-181c overexpresssion. [score:5]
We observed that miR-181c expression was not increased in several animals that were followed for 3 weeks after the completion of treatment, and the transient nature of miR overexpression with nanovector treatment has been reported previously [13]. [score:5]
Despite complex IV remo deling and reduction in the expression of key subunits following miR-181c overexpression, overall mitochondrial function and membrane potential are well maintained because of an increase in matrix [Ca [2+]], which increases the activity of other electron transport components. [score:5]
There are multiple novel aspects of this study, which further reveal mechanistic insights concerning the pathophysiologic effects of prolonged miR-181c overexpression, involving mitochondrial gene regulation, in-vivo. [score:4]
We showed that miR-181c, derived from the nuclear genome, translocates to the mitochondria, and more importantly, regulates mitochondrial gene expression and affects mitochondrial function [11]. [score:4]
Our work shows that miRNA can regulate mitochondrial gene expression, specifically that miR-181c binds to the 3′-end of the mRNA of a mitochondrial gene, mt-COX1, a subunit of complex IV of the respiratory chain, and initially results in a decrease in mt-COX1 protein, complex IV remo deling, and increased production of reactive oxygen species [11]. [score:4]
After only 2 boluses of Ca [2+], the mitochondria released the accumulated Ca [2+] in the miR-181c overexpression group, indicating mPTP opening, whereas it took the sham group 8 additional Ca [2+] pulses before Ca [2+] release occurred. [score:3]
Overexpression of miR-181c significantly increased the rate of ROS generation in the miR-181c -treated group (Fig. 6B). [score:3]
One explanation for this high ΔΨ [m] would be if miR-181c overexpression causes mitochondrial matrix Ca [2+] concentration to increase [18], [19] and this activates calcium-sensitive mitochondrial dehydrogenases [19], [20]. [score:3]
Although we did not find any sign of hypertrophy (Fig. 3C), using echocardiography, we find that miR-181c overexpression causes a significant decrease in left ventricular fractional shortening (FS) and markedly lower ejection fraction (EF) (Fig. 4A–C). [score:3]
But, using glutamate/malate (complex I) and succinate (complex II), ROS production is significantly higher in the miR-181c overexpression groups. [score:3]
Thus there are potential detrimental effects of the increase in matrix calcium, and the increase in ROS, that occurs with miR-181c overexpression. [score:3]
These data suggest that miR-181c overexpression in vivo has progressive effects on mitochondrial complex IV. [score:3]
0096820.g005 Figure 5 (A) qPCR data show that overexpression of miR-181c significantly reduces the mRNA levels of all mitochondrial complex IV genes with 3 weeks treatment. [score:3]
n = 3. (C) Western blot shows that miR-181c overexpression significantly increases the protein content of the mitochondrial calcium uniporter (MCU) both from total heart homogenate and mitochondrial fraction. [score:3]
Systemic miR-181c delivery target mitochondrial gene in the heart. [score:3]
This likely reflects the longer duration of miR-181c overexpression in our in vivo protocol. [score:3]
In vivo, we did not see a significant change either in miR-181c expression (Fig. S2 in File S1), or in mRNA levels of mt-COX1 or mt-COX2 in the heart at 2 weeks; however, we did observe a significantly higher level of mt-COX3. [score:3]
One of the key findings of this study is that overexpression of miR-181c leads to dysfunction of complex IV, which activates ROS generation and O [2] consumption; involving increased matrix [Ca [2+]]. [score:3]
We found that COX 5A and COX 5B are not significantly altered by chronic miR-181c overexpression in vivo. [score:3]
The nanovector is an electrostatic complex of positively charged liposomal nanoparticles and negatively charged plasmid DNA (in this case, expressing miR-181c) [13]. [score:3]
Our data suggest that complex IV remo deling affects more than just the subunits that are products of the mitochondrial genome and subject to direct regulation by miR-181c within the mitochondrial matrix. [score:3]
To investigate possible mechanisms to explain the increase in matrix calcium, we examined the expression of the mitochondrial calcium uniporter (MCU), and found that MCU expression was increased in the miR-181c treatment group (Fig. 7D). [score:3]
3 weeks after treating the rats with nanoparticles with/without miR-181c expression vector, we stained sections of five different organs with hematoxylin and eosin (H&E). [score:3]
We have observed a significant decrease in the protein content of COX VIIa in the miR-181c overexpression groups, but no effect on COX 5A and COX 5B. [score:3]
0096820.g003 Figure 3(A) miR-181c expression in the Heart and in the Heart-derived Mitochondrial Fraction. [score:3]
In fact, like our miR-181c overexpressor mo del, the role of ROS and Ca [2+] in the pathogenesis of myocardial stunning is well documented [31], [33]; including mitochondrial matrix [Ca [2+]] overload [34]. [score:3]
This differs from our earlier in-vitro [11] work, in which, after 48 hr of miR-181c overexpression, we observed a significant decrease in mt-COX1 protein levels, but a significant increase in mt-COX2 protein levels. [score:3]
0096820.g004 Figure 4 (A) 2D M-mode and Doppler echocardiography was performed on non-anesthetized rats, before (top) and after (lower) the sham (left) or the miR-181c expression vector (right) treatment. [score:3]
miR-181c expression constructs. [score:3]
The effect of miR-181c overexpression using nanovector delivery is transient. [score:3]
The nanovector is an electrostatic complex of positively-charged liposomal nanoparticles and negatively-charged plasmid Nucleotide, and was prepared by mixing pMSCV-Neo vectors expressing miR-181c and liposome on a 1∶3 Nucleotide/lipid charge ratio basis. [score:3]
qPCR shows that miR-181c expression is almost 2.5 times higher in the miR-181c -treated group compared to its sham group. [score:2]
Overexpression of miR-181c markedly increases respiration compared to the sham, after adding TMPD/Ascorbate. [score:2]
miR-181c overexpression shows a significant difference in exercise capacity compared to the sham group after the 18th day of treatment. [score:2]
As we saw in our in-vitro study [11], the rate of O [2] consumption is significantly increased in miR-181c overexpressing mitochondria compared to the sham after adding complex IV substrate (Fig. 6A). [score:2]
qPCR shows that miR-181c expression in the whole heart homogenate is almost 1.5 times higher in the plasmid miR-181c group compared to its sham group. [score:2]
Systemic miR-181c delivery regulates Mitochondrial Function. [score:2]
As shown in Figure 7B-C, mitochondria derived from miR-181c -treated hearts have a reduced ability to accumulate and retain Ca [2+] and are very susceptible to mPTP opening with Ca [2+] addition. [score:1]
Mitochondrial Complex IV Remo deling after miR-181c Treatment. [score:1]
We measured the expression of miR-181c in the heart, and found a ∼2 fold increase (Fig. 3A). [score:1]
Rats were weighed during the treatment period, and we found that the weight gain of miR-181c -treated rat group is significantly lower than the sham group, up to day 11. [score:1]
The miR-181c treatment group showed a higher level of TMRE intensity before the CCCP addition. [score:1]
We observed that miR-181c overexpression groups are more physically active and gain less weight during the first 2 weeks of the treatment (Fig. 2B); we measured serum and urine glucose and found no evidence that the animals were diabetic. [score:1]
It appears that only complex IV is altered since we have measured ND2 and ATPase 8 mRNA levels and have not found any changes with miR-181c overexpression (Fig. S1 in File S1). [score:1]
Preparation of nanovector for systemic miR-181c delivery in the rats. [score:1]
The red bar indicates the plasmid miR-181c treated group, and the blue bar indicates the sham group. [score:1]
Effect of miR-181c in different organs by systemic delivery. [score:1]
Effect of miR-181c on Mitochondrial Function. [score:1]
miR-181c and 361 bp of flanking sequence was amplified from rat genomic DNA using polymerase, and cloned into the EcoRI and XhoI sites of the MSCV-Neo vector (Clontech Laboratories). [score:1]
In the present study, we examined whether this in vitro finding is applicable in vivo, using a novel miR-181c delivery system using lipid based cationic nanoparticles [13]. [score:1]
But after day 13, miR-181c -treated animals become lethargic. [score:1]
Systemic miR-181c delivery with nanovectors shows signs of heart failure. [score:1]
These data show the role of miR-181c on mitochondrial energy metabolism by altering complex IV. [score:1]
We next assessed the functional consequences of translocation of miR-181c into the mitochondria. [score:1]
Unlike our in-vitro data, this in vivo (day 22) data suggests that miR-181c significantly decreases the mRNA and protein content of multiple complex IV mitochondrial genes (mt-COX1, mt-COX2 and mt-COX3) (Fig. 5A, 5B). [score:1]
, miR-181c) in the heart and its physiologic relevance in-vivo. [score:1]
Although the miR-181c -treated mitochondria are fully energized, an increase in matrix Ca [2+] may have detrimental effects on the ability of mitochondria to take up and retain additional Ca [2+], and may make the mitochondria more susceptible to opening of the mitochondrial permeability transition pore. [score:1]
We also observed that the miR-181c -treated group develops fatigue much earlier during exercise than the sham group. [score:1]
The red color indicates the plasmid miR-181c treated group, and the blue color indicates the sham group. [score:1]
The ratio of heart weight to tibial length is not different among the groups, suggesting no sign of hypertrophy in the miR-181c -treated rats. [score:1]
After pilot in vivo studies using several doses and different time-points, we optimized a 4 mg/kg dose of plasmid DNA, which increases miR-181c levels in heart tissue ∼2 fold with 6 injections over 3 weeks. [score:1]
We had previously found that endogenous miR-181c localizes to mitochondria [11], so we isolated RNA from the mitochondria [11] of the hearts treated with nanovector in vivo, and the miR-181c -treated group shows a significantly higher level of miR-181c in the heart-derived mitochondria (Fig. 3B). [score:1]
Thus despite reduced activity of complex IV, respiration is overall higher in the miR-181c -treated group (Fig 6A). [score:1]
Using a forced swimming test [14], we have found that the miR-181c -treated animals could only swim for 7–9 minutes on the 20th day of the treatment, whereas the sham group could swim the entire 20 minutes without any sign of fatigue (Fig. 2C). [score:1]
In vivo characterization of nanovectors for systemic miR-181c deliveryThe nanovector is an electrostatic complex of positively charged liposomal nanoparticles and negatively charged plasmid DNA (in this case, expressing miR-181c) [13]. [score:1]
The increase in ROS production in isolated heart mitochondria from the miR-181c -treated group provides a partial explanation for the increase in O [2] consumption. [score:1]
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3
[+] score: 64
Other miRNAs from this paper: hsa-mir-17, hsa-mir-18a, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-20a, hsa-mir-21, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-27a, hsa-mir-30a, hsa-mir-32, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-93, hsa-mir-107, hsa-mir-129-1, hsa-mir-30c-2, hsa-mir-139, hsa-mir-181c, hsa-mir-204, hsa-mir-212, hsa-mir-181a-1, hsa-mir-222, hsa-mir-15b, hsa-mir-23b, hsa-mir-132, hsa-mir-138-2, hsa-mir-140, hsa-mir-142, hsa-mir-129-2, hsa-mir-138-1, hsa-mir-146a, hsa-mir-154, hsa-mir-186, rno-mir-324, rno-mir-140, rno-mir-129-2, rno-mir-20a, rno-mir-7a-1, rno-mir-101b, hsa-mir-29c, hsa-mir-296, hsa-mir-30e, hsa-mir-374a, hsa-mir-380, hsa-mir-381, hsa-mir-324, rno-mir-9a-1, rno-mir-9a-3, rno-mir-9a-2, rno-mir-15b, rno-mir-17-1, rno-mir-18a, rno-mir-19b-1, rno-mir-19b-2, rno-mir-19a, rno-mir-21, rno-mir-23a, rno-mir-23b, rno-mir-24-1, rno-mir-24-2, rno-mir-27a, rno-mir-29c-1, rno-mir-30e, rno-mir-30a, rno-mir-30c-2, rno-mir-32, rno-mir-92a-1, rno-mir-92a-2, rno-mir-93, rno-mir-107, rno-mir-129-1, rno-mir-132, rno-mir-138-2, rno-mir-138-1, rno-mir-139, rno-mir-142, rno-mir-146a, rno-mir-154, rno-mir-186, rno-mir-204, rno-mir-212, rno-mir-181a-1, rno-mir-222, rno-mir-296, rno-mir-300, hsa-mir-20b, hsa-mir-431, rno-mir-431, hsa-mir-433, rno-mir-433, hsa-mir-410, hsa-mir-494, hsa-mir-181d, hsa-mir-500a, hsa-mir-505, rno-mir-494, rno-mir-381, rno-mir-409a, rno-mir-374, rno-mir-20b, hsa-mir-551b, hsa-mir-598, hsa-mir-652, hsa-mir-655, rno-mir-505, hsa-mir-300, hsa-mir-874, hsa-mir-374b, rno-mir-466b-1, rno-mir-466b-2, rno-mir-466c, rno-mir-874, rno-mir-17-2, rno-mir-181d, rno-mir-380, rno-mir-410, rno-mir-500, rno-mir-598-1, rno-mir-674, rno-mir-652, rno-mir-551b, hsa-mir-3065, rno-mir-344b-2, rno-mir-3564, rno-mir-3065, rno-mir-1188, rno-mir-3584-1, rno-mir-344b-1, hsa-mir-500b, hsa-mir-374c, rno-mir-29c-2, rno-mir-3584-2, rno-mir-598-2, rno-mir-344b-3, rno-mir-466b-3, rno-mir-466b-4
These miRNAs were chosen as representative of the different patterns that were observed: up-regulation (miR-21-5p) or down-regulation (miR-222-3p) during latency; up-regulation (miR-181c-5p) or down-regulation (miR-500-3p) in the chronic period; up-regulation (miR-146a-5p) or down-regulation (miR-551b-3p) in the entire course of the disease. [score:21]
Continuing modifications in the expression pattern of miRNAs in the course of chronic epilepsy support the hypothesis that epileptogenesis is a dynamic process that continues even after the initial diagnosis of the disease, i. e. after the initial spontaneous seizures 1. The comparison between chronic epileptic rats and the human cases identified four miRNAs (miR-21-5p, miR-23a-5p, miR-146a-5p and miR-181c-5p) that are similarly up-regulated in expression levels in both species. [score:10]
Continuing modifications in the expression pattern of miRNAs in the course of chronic epilepsy support the hypothesis that epileptogenesis is a dynamic process that continues even after the initial diagnosis of the disease, i. e. after the initial spontaneous seizures 1. The comparison between chronic epileptic rats and the human cases identified four miRNAs (miR-21-5p, miR-23a-5p, miR-146a-5p and miR-181c-5p) that are similarly up-regulated in expression levels in both species. [score:10]
Some miRNAs (miR-129-1-3p; miR-129-2-3p, miR-129-5p, miR181c-5p, miR181d-5p, miR-409a-5p, miR-655 and miR-874-3p) were up-regulated (Fig. 2, Supplementary Fig. S3A), whereas others (miR-296-5p, miR-500-3p and miR-652-3p) were down-regulated only in the chronic phase, while not being significantly altered during latency (Fig. 2, Supplementary Fig. S3B). [score:7]
Second, the chronic phase was accompanied by significant alterations in miRNA expression in the rat GCL, and comparison with data from epileptic patients identified several miRNAs (notably miR-21-5p, miR-23a-5p, miR-146a-5p and miR-181c-5p) that were up-regulated in both human and rat epileptic hippocampus. [score:6]
We identified four miRNAs (miR-21-5p, miR-23a-5p, miR-146a-5p and miR-181c-5p) that were up-regulated in both epileptic humans and rats (Table 1). [score:4]
Even if displaying the same patterns observed with the microarray, the expression levels of mir-181c-5p, miR-433-3p, miR-505-3p and miR-551b-3p were not significantly different from controls (Fig. 4). [score:3]
Cluster 4 included miR-181c-5p and miR-181d-5p. [score:1]
As for miR-181c-5p, it was highlighted by network analysis in cluster 4, and implicated in cytokine-cytokine receptor interaction and in the inflammatory response. [score:1]
Cluster 3 (that includes miR-142-3p and miR-146a-5p) and cluster 4 (including miR-181c-5p and miR-181c-5p) are connected to the “cytokine-cytokine receptor interaction” signaling pathway, which suggests a neuroinflammatory role for those miRNAs. [score:1]
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4
[+] score: 24
At the same time, up-regulation of hsa-miR-181c and hsa-miR-182 targets HRB and IGF1R expression, suggesting the biological functions of the two key genes may be suppressed. [score:10]
In contrast, the miRNAs hsa-miR-340 (14 degrees), hsa-miR-181c (11 degrees) and hsa-miR-182 (10 degrees) were significantly up-regulated in the DCM samples. [score:4]
In addition, has-miR-181c and has-miR-10a showed a trend towards higher expression levels in DCM samples (P > 0.05). [score:3]
Androulidaki et al. [36] found that miRNA-181c was involved in the lipopolysaccharide role of the macrophage inflammatory reaction by regulating Akt1. [score:2]
In addition, hsa-miR-181c (P > 0.05) and hsa-miR-10a (P > 0.05) exhibited a trend of higher expression levels in DCM samples, but these differences did not reach statistical significance when compared with control samples (Fig. 9). [score:2]
The key miRNAs identified included hsa-miR-181c, hsa-miR-19a and hsa-miR-19b, which all have higher degrees in the network diagram. [score:1]
Selected miRNAs (hsa-miR-10a, miR-19b, miR-181c, miR-302d and miR-340) were further quantified with TaqMan qRT-PCR. [score:1]
The miRNAs hsa-miR-200b (16 degrees), hsa-miR-181c (14 degrees), hsa-miR-340 (13 degrees), hsa-miR-557 (13 degrees), hsa-miR-19a (12 degrees), hsa-miR-19b (12 degrees) and hsa-miR-548f (12 degrees) were significantly differentially regulated in DCM samples compared with non-failing control samples. [score:1]
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5
[+] 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: 22
The expression levels of miRNAs miR-107, miR-181c, miR-103, miR-101, miR-29a, miR-21 and miR-9 expression levels were down-regulated in the serum of diabetic rats and IOMe -injected rats (A). [score:8]
0172429.g005 Fig 5 The expression levels of miRNAs miR-107, miR-181c, miR-103, miR-101, miR-29a, miR-21 and miR-9 expression levels were down-regulated in the serum of diabetic rats and IOMe -injected rats (A). [score:8]
The expression levels of miR-107, miR-181c, miR-103, miR-101, miR-29a, miR-21 and miR-9 were significantly down regulated in the blood serum of diabetic and IOMe -injected rats (Fig 5A) whereas, the expression levels of these miRNAs are normally high. [score:6]
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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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8
[+] score: 10
[50] MiR-101a, miR-124, miR-721, miR-181c and miR-365 target ERK/MAPK1, a gene involved in several physiological functions in brain including cell proliferation, differentiation and cell survival. [score:3]
Several components of PI3 kinase signaling such as AKT3, PTEN, PIK3C2A and PIK3C2, which play critical roles in neurotrophin -mediated signaling and cell survival, [62] are targets of miR-29a, miR-101a, miR-124, miR-181c and miR-678. [score:3]
As listed in Supplementary Table 6, these genes were predicted targets of miR-124, miR-101, miR-29a, miR-30e, miR-181c, miR-365 and miR-218. [score:3]
These include: AKT1 (miR-101a, miR-124, miR-181c, 29a, 365), BCL2 (153, 30e, 365), BDNF (124, 30e, 365), CREB (101a, 124, 721, 181c, 203, 218, 582-5p, 351, 155, 200c), DNMT3A (101a, 29a, 30e), ETS (351, 155, 200c), GABAR1 (101a, 721, 137, 181c, 155, 203), GRIA4 (124, 137, 218), GSK3B (155, 101a, 124, 137, 19b, 218, 29a), MAPK1 (miR-101a, 124, 721, 181c, 365), NR3C1(29a, 30e, 365, 582-5p, 124), phosphodiesterase 4 (PDE4a) (101A, 124, 137, 19B) and PDE4D (101a, 124, 721, 137, 30e, 365). [score:1]
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9
[+] score: 10
On day 7, miR-31, miR-214, miR-199a-5p, and miR-199a-3p were up-regulated, whereas miR-181c, miR-29b, miR-26b, miR-181d, mir-126, mir-499-5p, and miR-1 were down-regulated. [score:7]
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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10
[+] score: 9
Functional enrichment of predicted targets of both miRNAs indicates enrichment in GO terms for tissue morphology, nervous system development and cellular development, which was confirmed by in vitro inhibition of miR-181c [54]. [score:7]
We also see a trend towards a significant increase in miR-181c-5p (1.4 fold increase) in our sequencing data (Additional file 1: Table S1), which may be contributing to the gross morphological changes seen in GF mice. [score:1]
Administration of valproic acid coincides with an enlarged amygdala and increased miR-30d and miR-181c (~ 1.2 fold increase). [score:1]
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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
A subset of the rapidly down-regulated miRNA (miR-34a-5p, miR-34c-5p, miR-132-3p, miR-181c-5p, miR-214-3p) were chosen for more in-depth analysis by RT-qPCR, based on previous associations with plasticity processes (Wayman et al., 2008; Schonrock et al., 2010; Agostini et al., 2011; Zovoilis et al., 2011; Ryan et al., 2012). [score:4]
Using individual TaqMan qPCR assays, we confirmed reduced expression of miR-34a-5p and miR-132-3p (miR-34a-5p: p = 0.0001, n = 8; miR-132-3p: p = 0.001, n = 8; Figure 3), but not miR-34c-5p (p = 0.14, n = 9), miR-181c-5p (p = 0.46, n = 10) or miR-214-3p (p = 0.65, n = 9). [score:2]
Most changes were modest in magnitude, with two–thirds showing a fold change less than ±0.40 and only four miRNA (miR-181c-5p, miR-19b-3p, miR-218a-5p, miR-9a-5p) showing more than a twofold change. [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-181a-2, 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
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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15
[+] score: 6
MicroRNA-181c negatively regulates the inflammatory response in oxygen-glucose-deprived microglia by targeting Toll-like receptor 4. J. Neurochem. [score:3]
The microRNA miR-181c controls microglia -mediated neuronal apoptosis by suppressing tumor necrosis factor. [score:3]
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16
[+] 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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17
[+] score: 5
Some miRNAs which have been previously reported to be involved in brain disorders and drug abuse, including miR-133b, miR-134, miR-181c, miR-191, miR-22, miR-26b, miR-382, miR-409-3p and miR-504, were found to be changed in their expression following repeated cocaine exposure and subsequent abstinence from cocaine treatment. [score:3]
Other miRNAs, such as miR-181c, miR-191, miR-22, miR-99b*, and miR-369-5p, are also differentially modulated in rat hippocampus during post-status epilepsy [21, 22]. [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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18
[+] 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-181a-2, rno-mir-181b-1, rno-mir-181b-2, rno-mir-194-1, rno-mir-194-2, rno-mir-208a, rno-mir-181a-1, hsa-mir-423, hsa-mir-18b, hsa-mir-20b, hsa-mir-451a, mmu-mir-451a, rno-mir-451, ssc-mir-122, ssc-mir-15b, ssc-mir-181b-2, ssc-mir-19a, ssc-mir-20a, ssc-mir-26a, ssc-mir-326, ssc-mir-181c, ssc-let-7c, ssc-let-7f-1, ssc-let-7i, ssc-mir-18a, ssc-mir-29c, ssc-mir-30c-2, hsa-mir-484, hsa-mir-181d, hsa-mir-499a, rno-mir-1, rno-mir-133b, mmu-mir-484, mmu-mir-20b, rno-mir-20b, rno-mir-378a, rno-mir-499, hsa-mir-378d-2, mmu-mir-423, mmu-mir-499, mmu-mir-181d, mmu-mir-18b, mmu-mir-208b, hsa-mir-208b, rno-mir-17-2, rno-mir-181d, rno-mir-423, rno-mir-484, mmu-mir-1b, ssc-mir-15a, ssc-mir-16-2, ssc-mir-16-1, ssc-mir-17, ssc-mir-130a, ssc-mir-101-1, ssc-mir-101-2, ssc-mir-133a-1, ssc-mir-1, ssc-mir-181a-1, ssc-let-7a-1, ssc-let-7e, ssc-let-7g, ssc-mir-378-1, ssc-mir-133b, ssc-mir-499, ssc-mir-143, ssc-mir-423, ssc-mir-181a-2, ssc-mir-181b-1, ssc-mir-181d, ssc-mir-98, ssc-mir-208b, ssc-mir-142, ssc-mir-19b-1, hsa-mir-378b, ssc-mir-22, rno-mir-126b, rno-mir-208b, rno-mir-133c, hsa-mir-378c, ssc-mir-194b, ssc-mir-133a-2, ssc-mir-484, ssc-mir-30c-1, ssc-mir-126, ssc-mir-378-2, ssc-mir-451, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, mmu-mir-378b, mmu-mir-101c, hsa-mir-451b, hsa-mir-499b, ssc-let-7a-2, ssc-mir-18b, hsa-mir-378j, rno-mir-378b, mmu-mir-133c, mmu-let-7j, mmu-mir-378c, mmu-mir-378d, mmu-mir-451b, ssc-let-7d, ssc-let-7f-2, ssc-mir-20b-1, ssc-mir-20b-2, ssc-mir-194a, mmu-let-7k, mmu-mir-126b, mmu-mir-142b, rno-let-7g, rno-mir-15a, ssc-mir-378b, rno-mir-29c-2, rno-mir-1b, ssc-mir-26b
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: 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-181a-2, 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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21
[+] 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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22
[+] 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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23
[+] score: 3
In order to determine if this ethanol effect showed specificity for let-7b, we assessed two additional relevant pro-inflammatory miRNAs, miR-155 and miR181c. [score:1]
HMGB1 binding to miR181c was non-detectable after ethanol treatment (not shown). [score:1]
let-7b, miR-155, and miR181c were assessed as described above. [score:1]
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24
[+] 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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25
[+] 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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26
[+] 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
To confirm the deep sequencing results, we used qRT-PCR to assess the expressions of 10 of the miRNAs (miR-183-5p, miR-9a-5p, miR-199a-5p, miR-351-5p, miR200b-3p, miR-191a-3p, miR-181c-3p, miR-330-5p, miR-126a-5p and miR-351-3p) in the 12-pair plasma samples from the hyperoxia rats and controls. [score:3]
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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: 2
Other miRNAs from this paper: hsa-let-7a-2, hsa-let-7c, hsa-let-7e, hsa-mir-15a, hsa-mir-16-1, hsa-mir-21, hsa-mir-22, hsa-mir-23a, hsa-mir-24-2, hsa-mir-100, hsa-mir-29b-2, mmu-let-7i, mmu-mir-99b, mmu-mir-125a, mmu-mir-130a, mmu-mir-142a, mmu-mir-144, mmu-mir-155, mmu-mir-183, hsa-mir-196a-1, mmu-mir-199a-1, hsa-mir-199a-1, mmu-mir-200b, hsa-mir-148a, mmu-mir-143, hsa-mir-181c, hsa-mir-183, hsa-mir-199a-2, hsa-mir-199b, hsa-mir-181a-1, hsa-mir-200b, mmu-mir-298, mmu-mir-34b, hsa-let-7i, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-130a, hsa-mir-142, hsa-mir-143, hsa-mir-144, hsa-mir-125a, mmu-mir-148a, mmu-mir-196a-1, mmu-let-7a-2, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-mir-15a, mmu-mir-16-1, mmu-mir-21a, mmu-mir-22, mmu-mir-23a, mmu-mir-24-2, rno-mir-148b, mmu-mir-148b, hsa-mir-200c, hsa-mir-155, mmu-mir-100, mmu-mir-200c, mmu-mir-181a-1, mmu-mir-29b-2, mmu-mir-199a-2, mmu-mir-199b, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-181c, hsa-mir-34b, hsa-mir-99b, hsa-mir-374a, hsa-mir-148b, rno-let-7a-2, rno-let-7c-1, rno-let-7c-2, rno-let-7e, rno-let-7i, rno-mir-21, rno-mir-22, rno-mir-23a, rno-mir-24-2, rno-mir-29b-2, rno-mir-34b, rno-mir-99b, rno-mir-100, rno-mir-124-1, rno-mir-124-2, rno-mir-125a, rno-mir-130a, rno-mir-142, rno-mir-143, rno-mir-144, rno-mir-183, rno-mir-199a, rno-mir-200c, rno-mir-200b, rno-mir-181a-1, rno-mir-298, hsa-mir-193b, hsa-mir-497, hsa-mir-568, hsa-mir-572, hsa-mir-596, hsa-mir-612, rno-mir-664-1, rno-mir-664-2, rno-mir-497, mmu-mir-374b, mmu-mir-497a, mmu-mir-193b, mmu-mir-466b-1, mmu-mir-466b-2, mmu-mir-568, hsa-mir-298, hsa-mir-374b, rno-mir-466b-1, rno-mir-466b-2, hsa-mir-664a, mmu-mir-664, rno-mir-568, hsa-mir-664b, mmu-mir-21b, mmu-mir-21c, rno-mir-155, mmu-mir-142b, mmu-mir-497b, rno-mir-148a, rno-mir-15a, rno-mir-193b
Cluster Mapped ESTs Mapped cDNAs mir-497~195 Human: CR737132, DB266639, DA2895925, BI752321, AA631714 Human: AK098506.1 Rat: CV105515 mir-144-451 Human: R28106 Mouse: AK158085.1 Rat: AW919398, BF2869095, AI008234 mir-99b~let-7e~mir-125a Human: DB340912 Human: AK125996 mir-143~145 Human: BM702257 mir-181a-1~181b-1 Human: DA528985, BX355821 Mouse: BE332980, CA874578 mir-29b-2~29c Human: BF089238 Mouse: AK081202, BC058715 mir-298~296 Human: W37080 mir-183~96~182 Human: CV424506 mir-181c~181d Human: AI801869, CB961518, CB991710, BU729805, CB996698, BM702754 Mouse: CJ191375 mir-100~let-7a-2 Human: DA545600, DA579531, DA474693, DA558986, DA600978 Human: AK091713 Mouse: BB657503, BM936455 Rat: BF412891, BF412890, BF412889, BF412895 Mouse: AK084170 mir-374b~421 Human: DA706043, DA721080 Human: AK125301 Rat: BF559199, BI274699 Mouse: BC027389, AK035525, BC076616, AK085125 mir-34b~34c Human: BC021736 mir-15a-16-1 Human: BG612167, BU932403, BG613187, BG500819 Human: BC022349, BC022282, BC070292, BC026275, BC055417, AF264787 Mouse: AI789372, BY718835 Mouse: AK134888, AF380423, AF380425, AK080165 mir-193b~365-1 Human: BX108536 hsa-mir-200c~141 Human: AI969882, AI695443, AA863395, BM855863.1, AA863389 mir-374a~545 Human: DA685273, AL698517, DA246751, DA755860, CF994086, DA932670, DA182706 Human: AK057701 Figure 2 Predicted pri-miRNAs, their lengths, and features that support the pri-miRNA prediction. [score:1]
Cluster Mapped ESTs Mapped cDNAs mir-497~195 Human: CR737132, DB266639, DA2895925, BI752321, AA631714 Human: AK098506.1 Rat: CV105515 mir-144-451 Human: R28106 Mouse: AK158085.1 Rat: AW919398, BF2869095, AI008234 mir-99b~let-7e~mir-125a Human: DB340912 Human: AK125996 mir-143~145 Human: BM702257 mir-181a-1~181b-1 Human: DA528985, BX355821 Mouse: BE332980, CA874578 mir-29b-2~29c Human: BF089238 Mouse: AK081202, BC058715 mir-298~296 Human: W37080 mir-183~96~182 Human: CV424506 mir-181c~181d Human: AI801869, CB961518, CB991710, BU729805, CB996698, BM702754 Mouse: CJ191375 mir-100~let-7a-2 Human: DA545600, DA579531, DA474693, DA558986, DA600978 Human: AK091713 Mouse: BB657503, BM936455 Rat: BF412891, BF412890, BF412889, BF412895 Mouse: AK084170 mir-374b~421 Human: DA706043, DA721080 Human: AK125301 Rat: BF559199, BI274699 Mouse: BC027389, AK035525, BC076616, AK085125 mir-34b~34c Human: BC021736 mir-15a-16-1 Human: BG612167, BU932403, BG613187, BG500819 Human: BC022349, BC022282, BC070292, BC026275, BC055417, AF264787 Mouse: AI789372, BY718835 Mouse: AK134888, AF380423, AF380425, AK080165 mir-193b~365-1 Human: BX108536 hsa-mir-200c~141 Human: AI969882, AI695443, AA863395, BM855863.1, AA863389 mir-374a~545 Human: DA685273, AL698517, DA246751, DA755860, CF994086, DA932670, DA182706 Human: AK057701 Figure 2 Predicted pri-miRNAs, their lengths, and features that support the pri-miRNA prediction. [score:1]
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Among these miRNAs, miRNAlet-7a, miRNA-124, and miRNA-137 were reported to induce neuroprotection after cerebral ischemia, while miRNA-34a, microRNA-181c, and miRNA-17–92 were reported to exacerbates brain injury in ischemic Stroke (Szulwach et al., 2010; Liu et al., 2013; Hamzei Taj et al., 2016; Liang and Lou, 2016; Ma et al., 2016; Wang et al., 2016). [score:1]
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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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Bdnf has a large, 2.9 kb 3′UTR with multiple seed binding sites for several miRNAs differentially affected by TBI, miR-15b, miR-146b, miR-17-5p (all increased) and miR-181c (decreased). [score:1]
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Similarly to our findings in patients, the levels of miR-16 werenot changed but the levels of miR-181c were reducedin the CCH rats (Figure 2A, 2B). [score:1]
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Other miRNAs from this paper: hsa-mir-181c, hsa-mir-132, rno-mir-132, hsa-mir-1246
Brain metastatic cancer cells release microRNA-181c-containing extracellular vesicles capable of destructing blood-brain barrier. [score:1]
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9 -45.6 mmu-miR-27b -1.8 -71.4 -462.7 mmu-miR-214* -2.6 -5.0 -43.5 mmu-let-7c-1* -73.2 -204.4 -334.1 mmu-miR-34c -9.4 -26.1 -42.7 mmu-miR-542–3p -5.9 -195.6 -319.8 mmu-miR-706 -9.3 -5.0 -38.7 mmu-miR-487b -2.0 -161.5 -263.9 mmu-miR-467b* -10.1 -2.2 -33.6 rno-miR-17–3p -1.6 -152.0 -248.5 mmu-miR-323–3p -3.7 -23.3 -29.8 mmu-miR-10b -2. 4 -136.6 -223.3 mmu-miR-202–3p -6.5 -5.9 -21.4 mmu-miR-29b -3.0 -135.1 -220.9 mmu-miR-339–5p -1.6 -9.6 -19.6 mmu-miR-297a* -2.4 -128.4 -209.8 mmu-miR-181c -2.0 -10.5 -14.6 mmu-miR-692 -41.5 -115.8 -189.2 mmu-miR-203 -4.6 -6.4 -13.8 mmu-miR-208 -40.6 -113.5 -185.5 mmu-miR-467a* -2.6 -3.9 -11.4 mmu-miR-467c -38.9 -108.6 -177. [score:1]
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