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59 publications mentioning rno-mir-214

Open access articles that are associated with the species Rattus norvegicus and mention the gene name mir-214. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

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[+] score: 450
c Twist1 overexpression upregulated miR-214 expression and downregulated SUFU expression, and (d) the protein levels of profibrotic markers FN and α-SMA was upregulated by Twist1 in HSCs. [score:16]
e Twist1 overexpression upregulated miR-214 expression and downregulated SUFU expression, and f the protein level of profibrotic markers FN was upregulated by Twist1 in LX2. [score:16]
Importantly, Sufu expression was upregulated in response to antagomiR-214 treatment (Fig.   7g, h), suggesting that miR-214 suppression can modulate the expression of Sufu for the treatment of liver fibrosis and indicating miR-214 has a potential to be used as a therapeutic target in clinical studies for liver fibrosis. [score:12]
Relative expression levels are shown as the means ± s. e. m obtained from triplicate experiments (unpaired two-sample Student’s t test, * P < 0.05 and **P < 0.01) To explore the mechanism by which miR-214 regulates HSC activation and to identify the relevant target genes of miR-214, we conducted bioinformatics analyses using the commonly used software including TargetScan, miRBase, and miRanda, and found that Sufu, a downstream factor of Hedgehog signaling, could be a potential target of miR-214. [score:10]
Thus, increasing the expression of mature miR-214 which targets the 3′-UTR of Sufu to suppress its translation. [score:9]
In this study, we took advantage of rat primary HSCs and human LX2 cells for in vitro studies, and found that the knockdown of miR-214 expression in HSCs and LX2 cells using antagomiR-214 resulted in cell morphological changes, decreased expression of profibrotic genes, and inhibition of cell proliferation. [score:8]
Relative expression levels are shown as the means ± standard deviation obtained from triplicate experiments (unpaired two-sample Student’s t test, * P < 0.05 and ** P < 0.01) To study the functional relevance of miR-214 in fibrogenesis, we knocked down the expression of miR-214 using antagomiRs or overexpressed miR-214 using mimics in activated rat primary HSCs and human HSC cell line (LX2). [score:8]
Indeed, Sufu expression was reduced in the clinical cirrhosis tissues (Fig.   5j) and was negatively correlated with miR-214 expression, indicating that miR-214 regulates fibrogenesis by targeting Sufu to modulate the Hedgehog signal pathway. [score:8]
Both Lakner et al. [17] and Maubach et al. [26] took advantage of microarray technology to identify that miR-214 is upregulated during HSC activation, whereas Chen et al. [27] showed that miR-214 is downregulated. [score:7]
Moreover, luciferase assay indicated that miR-214 inhibited Sufu expression by directly targeting the 3′-UTR of Sufu mRNA (Fig.   4e, f). [score:7]
Functional studies demonstrated that miR-214 plays a pivotal role in hepatic fibrosis by regulating Sufu expression, and knockdown of miR-214 expression by antagomiRs effectively alleviate liver fibrosis in CCl [4] -treated mice. [score:7]
This indicated that Twist1 regulates the expression of miR-214, which indirectly affects Sufu levels and profibrotic markers expression in vitro. [score:7]
Intriguingly, miR-214 was one of the most significantly upregulated miRNA in aHSCs and its upregulation was further validated by real-time quantitative PCR (RT-qPCR) analysis (Fig.   1e). [score:7]
As expected, Twist1 overexpression resulted in a significant increase in miR-214 expression accompanied by a reduction in Sufu expression in HSCs (Fig.   6c) or LX2 cells (Fig.   6e). [score:7]
For example, miR-214 expression is upregulated in the renal fibrosis, and genetic deletion of miR-214 significantly attenuated kidney interstitial fibrosis induced by unilateral ureteral obstruction [30]. [score:6]
miR-214 expression is upregulated in different liver injury mo dels. [score:6]
To determine whether Twist1 regulates miR-214 expression in HSCs and in liver fibrosis mo dels, we overexpressed Twist1 in rat HSCs (Fig.   6a) or LX2 (Fig.   6b) using lentiviral vectors containing GFP. [score:6]
Conversely, the constructs with the mutated forms of 3′-UTR resulted in no significant change in luciferase activity in HEK 293T cells (Fig.   4f, g) or HSCs (Supplementary Fig.   3a and 3b), indicating that miR-214 influences Sufu expression by directly targeting the 3′-UTR of Sufu mRNA. [score:6]
In summary, we found that miR-214 expression is significantly upregulated during HSC activation and liver injury samples. [score:6]
Mechanistically, miR-214 enhances HSC activation by suppressing Sufu expression and thus regulates the Hedgehog signaling pathway. [score:6]
Twist1 was found to be upregulated during fibrosis 28, 29, which further supports that miR-214 expression increased during liver fibrosis. [score:6]
In this rat mo del of liver fibrosis, miR-214 expression was found to be upregulated in a manner dependent on the severity of liver fibrosis (Fig.   2c). [score:6]
Therefore, we overexpressed Twist1 to verify whether Twist1 also regulates miR-214 expression in HSCs. [score:6]
Moreover, we also showed that the expression of miR-214 was upregulated with the progression of hepatic fibrosis in CCl [4] -treated rat or mouse mo del, an HFD -induced NASH mouse mo del and in patients with cirrhosis (Fig.   2). [score:6]
These findings indicate that miR-214 has great potential to be used as a biomarker of hepatic fibrosis and a therapeutic target for treating liver diseases (Fig.   8). [score:5]
Furthermore, we observed high expression of Twist1 in clinical cirrhosis samples (Fig.   6g), which was positively correlated with miR-214 expression. [score:5]
Most importantly, we observed reduced Sufu expression in clinical cirrhosis liver samples, which was negatively correlated with miR-214 expression (Fig.   5). [score:5]
miR-214 regulates Sufu expression by direct binding to the 3′-UTR of its mRNA. [score:5]
Relative expression levels are shown as the means ± s. e. m obtained from triplicate experiments (unpaired two-sample Student’s t test, * P < 0.05 and **P < 0.01) a HSCs were transfected with either antagomiR-214 or NC-miR for 48 h, and the expression of miR-214 was detected by and b protein levels of FN and α-SMA were examined using Western blotting. [score:5]
All of these data suggested that Twist1 can indirectly affect fibrogenesis by upregulating miR-214. [score:5]
Following treatment, Sufu expression was upregulated due to decreased miR-214 level in the CCl [4]/antagomiR-214 group when compared with that in the CCl [4]/NC-miR group. [score:5]
The 3′-UTR region of rat and mouse Sufu mRNA containing the potential miR-214 binding site was cloned into pmirGLO Dual-Luciferase miRNA Target Expression Vector (Promega, Madison, WI, USA). [score:5]
In this study, we compared miRNA expression profiles between activated and quiescent HSCs (qHSCs) using microarray analysis and identified miR-214 as a significantly upregulated miRNA during HSC activation. [score:5]
However, qRT-PCR analysis demonstrated negligible effects of miR-214 on Sufu mRNA level (Fig.   4c, d), indicating that miR-214 may repress Sufu expression at the translational level. [score:5]
CCl [4] treatment induced miR-214 overexpression in mouse livers, which was markedly suppressed by antagomiR-214 (Fig.   7b). [score:5]
On the contrary, miR-214 overexpression promoted cell proliferation and induced profibrotic gene expression (Fig.   3 and Supplementary Fig.   2), thereby confirming that miR-214 takes part in the hepatic fibrogenesis. [score:5]
Using bioinformatics analysis, we identified Sufu, a well-known negative regulator of the Hedgehog pathway, as the potential target of miR-214. [score:4]
Mo del representing miR-214 regulates Sufu expression to participate in liver fibrogenesis. [score:4]
n. s. nonsignificant Based on the above data, we hypothesized that miR-214 affects fibrogenesis by regulating Sufu expression. [score:4]
To evaluate the therapeutic potential of miR-214 repression for anti-fibrosis in vivo, chemically synthesized antagomiR-214 oligos were injected into CCl [4] -treated mice to downregulate miR-214 expression in the liver. [score:4]
To investigate whether miR-214 directly target Sufu expression, we cloned the 3′-UTR sequences of rat or mouse Sufu mRNA into the luciferase reporter vector. [score:4]
miR-214 regulates fibrotic gene expression and promotes HSC cell proliferation. [score:4]
Sufu is a direct target of miR-214. [score:4]
In this study, we found that miR-214 was the most significantly upregulated miRNA during HSC activation (Fig.   1). [score:4]
Upregulation of miR-214 in different liver injury mo dels. [score:4]
As shown in Fig.   4a, b, Sufu expression clearly decreased in the cells transfected with miR-214 mimics compared with that in the control cells, while transfection with antagomiR-214 increased Sufu protein expression. [score:4]
This confirmed the regulation of miR-214 expression by Twist1 via the E-box element. [score:4]
Moreover, we conducted sited-directed mutagenesis to destroy the potential miR-214 binding site to further validate target specificity (Fig.   4e). [score:4]
Moreover, miR-214 expression is regulated by the transcriptional factor Twist1 through its binding to E-box element within the miR-214 promoter. [score:4]
Therefore, miR-214 plays a pivotal role in liver fibrosis by regulating Hedgehog signaling and may be used as a potential therapeutic target. [score:4]
Similar results were obtained in human LX2 cells by the knockdown (Supplementary Fig.   2a and 2b) or overexpression of miR-214 (Supplementary Fig.   2d and 2e). [score:4]
However, whether miR-214 regulates Sufu expression in HSCs and in liver fibrosis mo dels has not yet been examined. [score:4]
b data for miR-214 expression in livers from olive oil -treated, CCl [4]/NC-miR -treated, CCl [4]/antagomir-214 -treated mice (n = 5 per group). [score:3]
As expected, we found Twist1 induced the expression of miR-214 in HSCs and LX2 cells, respectively (Fig.   6c–f). [score:3]
Increased expression of miR-214 in activated HSCs. [score:3]
Since NASH has been recognized as a major cause of liver fibrosis [21], we examined miR-214 expression in the early stages of liver fibrosis. [score:3]
Taken together, our data clearly demonstrate that miR-214 has an important role in HSC activation and hepatic fibrosis through affecting Sufu expression. [score:3]
Fig. 3 a HSCs were transfected with either antagomiR-214 or NC-miR for 48 h, and the expression of miR-214 was detected by and b protein levels of FN and α-SMA were examined using Western blotting. [score:3]
GANT-61 is an inhibitor for Gli -induced transcript Transcription of miR-214 gene is induced by the binding of Twist1 with the E-box element in the promoter region of the miR-214 gene. [score:3]
In contrast, the overexpression of miR-214 via mimics increased the protein level of FN and α-SMA (Fig.   3c, d). [score:3]
Mutations within potential miR-214 binding sites were introduced by QuikChange Site-Directed Mutagenesis Kit (Life Technologies, Grand Island, NY, USA). [score:3]
Whether miR-214 expression increases or decreases during HSC activation is controversial. [score:3]
Luciferase activity was significantly repressed by the constructs harboring the wild-type rat or mouse miR-214 target sequence. [score:3]
Twist1 acts on an E-box elements to promote miR-214 expression in HSCs and LX2 cells. [score:3]
miR-214 expression was found to be significantly higher in human cirrhotic liver samples (Fig.   2f), and this was accompanied by high levels of FN protein (Supplementary Fig.   1e and 1f). [score:3]
miR-214 expression is increased during HSC activation. [score:3]
n. s. nonsignificant a, b Inverse correlation between miR-214 and Sufu expression in (a) rat primary HSCs and b human LX2 cells transfected with miR-214 mimics or antagomiR-214. [score:3]
n. s. nonsignificant To further confirm that miR-214 expression is driven by Twist1, we analyzed miR-214 promoter sequences and noted that the promoter contains E-box elements, which are known to be bound by Twist1 homodimers [24]. [score:3]
In addition, luciferase reporter assay results confirmed that Twist1 regulate miR-214 expression through the E-box element within the promoter (Fig.   6h, i). [score:3]
In contrast, overexpression of miR-214 could significantly promote cell growth in HSCs (Fig.   3g) and LX2 cells (Supplementary Fig.   2f). [score:3]
In this study, we identified that miR-214 effectively repressed Sufu expression in HSCs and LX2 cells (Fig.   4a, b). [score:3]
miR-214 -mediated fibrogenesis depends on Sufu expression. [score:3]
Masson’s trichrome and H&E staining clearly demonstrated that antagomiR-214 treatment effectively ameliorate liver fibrosis, implying that miR-214 is a therapeutic target for hepatic fibrosis treatment (Fig.   7). [score:3]
As expected, miR-214 expression was successfully reduced by antagomiR-214 in HSCs (Fig.   3a). [score:3]
The protein level of FN and α-SMA were significantly repressed following the inhibition of miR-214 in HSCs (Fig.   3b). [score:3]
HEK 293T cells were co -transfected with vectors containing either the wild-type (wt) or mutant (mut) target sites of Sufu and either miR-214 mimics or negative control (NC). [score:3]
Furthermore, cell growth was suppressed after the repression of miR-214 by antagomiR-214 in rat primary HSCs (Fig.   3e, f) and human LX2 (Supplementary Fig.   2c), which was accompanied by the decrease of cell numbers and the change of cell morphology (Supplementary Fig.   2g and 2h) in HSCs and LX2, respectively. [score:3]
c HSCs were transfected with miR-214 mimics or NC-miR for 48 h, and the expression of miR-214 was detected by and d the protein levels of FN and α-SMA were detected by Western blotting. [score:3]
Most importantly, Twist1 was high expression in patients with cirrhosis which was positively correlated with miR-214 level (Fig.   6g). [score:3]
Fig. 4 a, b Inverse correlation between miR-214 and Sufu expression in (a) rat primary HSCs and b human LX2 cells transfected with miR-214 mimics or antagomiR-214. [score:3]
Moreover, miR-214 expression is controlled by the transcription factor Twist1, which binds to E-box elements within the miR-214 promoter. [score:3]
n. s. nonsignificantTo further confirm that miR-214 expression is driven by Twist1, we analyzed miR-214 promoter sequences and noted that the promoter contains E-box elements, which are known to be bound by Twist1 homodimers [24]. [score:3]
miR-214 promotes expression of profibrotic markers and cell proliferation in HSCs and LX2 cells. [score:3]
e Differential expression of miR-214 in primary rat HSCs was validated using. [score:3]
These results indicated an increasing expression of miR-214 in aHSCs and suggested a key role of miR-214 in HSC activation. [score:3]
Twist1 affects liver fibrogenesis by regulating miR-214. [score:2]
The mutant miR-214 promoter containing 2-base point mutation (CATCTG → CACGTG) in the E-box site was generated and verified by DNA sequencing. [score:2]
Compared with that in the control mice, miR-214 expression was significantly increased in the mice with HFD -induced liver samples (Fig.   2e), similar to what was observed in the rat mo del of CCl [4] -induced liver fibrosis. [score:2]
Through luciferase assay and, we demonstrated that Twist1 bound to the E-box element within the promoter and induced miR-214 expression (Fig.   6). [score:2]
For the miR-214 knockdown study, HSCs and LX2 cells were transfected with antagomiR-214 or negative control (NC). [score:2]
Moreover, miR-214 has been reported to target the 3′-UTR of Sufu mRNA in human lung adenocarcinoma cells by luciferase assay [23]. [score:2]
Indeed, knockdown of miR-214 significantly increased the percentage of cells in the G1 phase and reduced the percentage of cells in S and G2 phases, indicating that miR-214 can influence cell cycle distribution in HSCs (Supplementary Fig.   2i–k). [score:2]
n. s. nonsignificant According to the above data, miR-214 plays a vital role in fibrogenesis in vitro. [score:1]
Values represent the means ± standard deviation (SD), * P < 0.05 and ** P < 0.01 In a systematic approach to identify the involvement of miR-214 in liver fibrosis, we employed a well-established rodent mo del of carbon tetrachloride (CCl [4]) -induced liver fibrosis [20]. [score:1]
However, further studies are needed to elucidate the overall function of miR-214 and the associated mechanisms in liver fibrosis. [score:1]
Several reports showed that miR-214 participated in fibrosis. [score:1]
However, the role of miR-214 in liver fibrosis is controversial according to the literatures. [score:1]
However, in accordance with miR-214 reduction, liver damage was obviously ameliorated in the CCl [4]/antagomiR-214 group mice (Fig.   7c, d), which was accompanied by a reduction in COL1α1 mRNA level (Fig.   7e) and decreased α-SMA levels, which as detected by immunohistochemistry (Fig.   7f). [score:1]
These results suggest that miR-214 may play a crucial role in the HSC activation and liver fibrosis. [score:1]
The level of miR-214 in liver tissues was examined via. [score:1]
The miR-214 promoter region was amplified by PCR from the genomic DNA of primary rat HSCs, and the resultant fragments were cloned into pGL4.27 vector (Promega, Madison, WI, USA) at XhoI and HindIII (New England Biolabs, Ipswich, MA, USA) sites. [score:1]
b The mRNA level of α-SMA and COL1α1 and c miR-214 level was detected in CCl [4] -treated rat liver sections at different time points. [score:1]
The analyses were performed on BD LSR flow cytometer (BD Biosciences, San Jose, CA, USA) For examining whether miR-214 directly target Sufu mRNA, pMir-Report-sufu reporter plasmids were co -transfected with miR-214 mimics or scramble into HEK 293T cells using Lipofectamine 2000 for 24 h. After transfection, both firefly and Renilla luciferase activities were measured by Dual-Luciferase Assays Kit (Promega, Madison, WI, USA). [score:1]
In the cardiac tissues, miR-214 is a sensitive marker of cardiac stress, and miR-214- deletion leads to increased fibrosis after ischemic injury [31]. [score:1]
Therefore, miR-214 likely plays a crucial role in the initiation or/and progression of liver fibrosis. [score:1]
Fig. 8Transcription of miR-214 gene is induced by the binding of Twist1 with the E-box element in the promoter region of the miR-214 gene. [score:1]
For investigating whether Twist1 binds to the promoter of miR-214 gene, the recombinant pGL4.27 plasmid containing wild-type or mutant miR-214 gene promoter was co -transfected into HEK 293T cells with Twist1 expression plasmid and pRL-TK containing Renilla luciferase reporter gene. [score:1]
These results demonstrated the functional relevance of miR-214 in fibrogenesis in vitro. [score:1]
To further understand the differences, we found that Chen et al. [27] normalized miR-214 expression to GAPDH mRNA while we normalized miR-214 levels to U6 RNA, a noncoding small nuclear RNA commonly used for miRNA measurement. [score:1]
c, d analyses of Sufu mRNA levels after transfection of miR-214 mimics or antagomiR in HSCs (c) and in LX2 cells (d). [score:1]
To this end, we transfected miR-214 mimics or antagomiR-214 into rat primary HSCs and human LX2 cells. [score:1]
AntagomiR-214 ameliorates liver fibrosis induced by CCl [4] in miceAccording to the above data, miR-214 plays a vital role in fibrogenesis in vitro. [score:1]
The sequence of mature miR-214 is identical in human, rat, and mouse, and bioinformatics analysis revealed that Sufu mRNAs have the potential miR-214 binding sites (Fig.   4e). [score:1]
Blue shading indicates the seed sequence of miR-214. [score:1]
f miR-214 expression in the liver of cirrhosis or healthy controls was measured by. [score:1]
e Potential miR-214 binding sites were predicted in the 3′-UTR of rat or mouse Sufu mRNAs. [score:1]
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[35] Moreover, our study implies that after transfection, miR-214 was down-regulated, Mfn2 was elevated, and there were elevated expression levels of N-cadherin, Fibronectin, Twist1, Snail and Vimentin and decreased expression levels of E-cadherin and ZO-1, thus further confirming the changes in expression levels of the EMT-related proteins, the reduced miR-214 expression and the increased Mfn2 expression. [score:14]
The ADMSCs at the logarithmic phase were obtained and randomly assigned to the following 7 groups: the blank group (A group; transfected with 100 nmol l [−1] empty plasmid), the miR-214 mimics group (B group; transfected with 100 nmol l [−1] miR-214 mimics plasmid), the miR-214 inhibitors group (C group; transfected with 100 nmol l [−1] miR-214 inhibitors plasmid), the mimics NC group (D group; transfected with 100 nmol l [−1] mimics NC plasmid), the inhibitor NC group (E group; transfected with 100 nmol l [−1] inhibitor NC plasmid), the Mfn2 siRNA group (F group; transfected with 100 nmol l [−1] Mfn2 siRNA plasmid), and the miR-214 inhibitors+Mfn2 siRNA group (G group; transfected with 100 nmol l [−1] miR-214 inhibitors plasmid and 100 nmol l [−1] Mfn2 siRNA plasmid). [score:13]
Once the cell density reached 70%, the cells were randomly assigned into the following 4 groups: the miR-214 mimics+Mfn2-3′-UTR-WT group (A group; transfected with 100 nmol l [−1] miR-214 mimics and the Mfn2-3′-UTR-WT plasmid), the miR-214 inhibitors+Mfn2-3′-UTR-WT group (B group; transfected with 100 nmol l [−1] miR-214 inhibitors and the Mfn2-3′-UTR-WT plasmid), the miR-214 mimics+100 Mfn2-3′-UTR-MUT group (C group; transfected with 100 nmol l [−1] miR-214 mimics and 100 nmol l [−1] Mfn2-3′-UTR-MUT plasmid), and the miR-214 inhibitors+Mfn2-3′-UTR-MUT group (D group; transfected with 100 nmol/l miR-214 inhibitors and the Mfn2-3′UTR-MUT plasmid). [score:9]
The rats were randomly assigned to the following 8 groups: the blank group (A group; transfected with an empty plasmid), the miR-214 mimics group (B group; transfected with the miR-214 mimics), the miR-214 inhibitors group (C group; transfected with the miR-214 inhibitors), the mimics NC group (D group; transfected with the mimics NC), the inhibitors NC group (E group; transfected with the inhibitors NC), the Mfn2 siRNA group (F group; transfected with the Mfn2 siRNA), the miR-214 mimics+Mfn2 siRNA group (G group; transfected with the miR-214 mimics and Mfn2 siRNA), and the normal saline (NS) group (H group; perfused with NS). [score:9]
These results further confirmed that inhibiting miR-214 could up-regulate Mfn2 expression, promote the EMT process and lead to fibrosis of the bladder wall, thereby inducing the occurrence of IC. [score:8]
The expression levels of E-cadherin and ZO-1 mRNA and protein increased, whereas those of N-cadherin, Fibronectin, Twist1, Snail and Vimentin mRNA and protein were down-regulated in the miR-214 inhibitors group. [score:8]
6, 7 Wang and his colleagues showed that there is down-regulation of miR-214 in bladder lesion tissues, suggesting that miR-214 could exert a tumor-suppressive influence in bladder cancer through directly down -regulating oncogene PDRG1, which may act as a promising indicator for prognostic and therapeutic interventions in bladder cancer. [score:8]
The qRT–PCR and western blotting results indicated that compared with the blank group, the expression levels of E-cadherin and ZO-1 mRNA and protein were up-regulated, whereas those of N-cadherin, Fibronectin, Twist1, Snail and Vimentin mRNA and protein down-regulated in the miR-214 mimics and Mfn2 siRNA groups. [score:8]
The findings of our study demonstrated that by targeting Mfn2, the suppression of miR-214 expression is able to promote the EMT process and contribute to bladder wall fibrosis, thus leading to IC in postmenopausal women. [score:7]
MiR-214 expression decreased, whereas Mfn2 mRNA expression increased in the miR-214 inhibitors group. [score:7]
Subsequently, when normal bladder tissues are treated with an exosome, the expression levels of Mfn2 and the EMT-related proteins significantly changed with increases in the expression of Mfn2, N-cadherin, Fibronectin, Twist1, Snail and Vimentin m -RNA and reductions in the expression of miR-214, E-cadherin and ZO-1 m -RNA. [score:7]
In normal bladder cells treated with exosomes and IC bladder cells, the expression of miR-214 and of E-cadherin and ZO-1 mRNA and protein significantly decreased, whereas the expression of Mfn2 mRNA and of N-cadherin, Fibronectin, Snail, Twist1 and Vimentin mRNA and protein increased compared with the expression observed in the normal bladder cells (all P<0.05). [score:6]
Our initial findings reveal that the main syndrome of IC is a chronic inflammation and fibrosis in the bladder, and Mfn2 is up-regulated while miR-214 is inhibited in the IC bladder tissues. [score:6]
The TargetScan online software was applied to predict the possible gene targeted of miR-214. [score:5]
These results indicated that the inhibition of miR-214 and the over -expression of Mfn2 could promote the EMT process and lead to bladder wall fibrosis, further inducing IC. [score:5]
Interestingly, when the exosome of each transfected group is injected into the bladder of a postmenopausal rat, chronic inflammation and fibrosis are observed, which further explains that the inhibition of miR-214 can enhance the EMT process in the pathogenesis of IC by targeting Mfn2. [score:5]
The expression levels of E-cadherin and ZO-1 mRNA and protein decreased, whereas those of N-cadherin, Fibronectin, Twist1, Snail, and Vimentin mRNA and protein increased in the miR-214 inhibitors group. [score:5]
Exosomes (0.5 ml per group) were injected into the rats’ bladders in the blank, miR-214 mimics, miR-214 inhibitors, mimics NC, inhibitors NC, Mfn2 siRNA and miR-214 mimics+Mfn2 siRNA groups, while NS (0.5 ml) was injected and stored in the rats’ bladders for 30 min in the NS group. [score:5]
No significant difference was found among the Mfn2-3′-UTR-WT+miR-214 inhibitors, Mfn2-3′-UTR-MUT+miR-214 mimics and Mfn2-3′-UTR-MUT+miR-214 inhibitors groups (all P>0.05; Figure 7). [score:5]
An increase in Mfn2 expression was observed in the miR-214 inhibitors group. [score:5]
The results of the IHC staining and qRT-PCR indicated that the expression levels of Mfn2 mRNA and protein were higher but that the relative expression of miR-214 was lower in the IC tissues than those in the adjacent normal bladder tissues (Figure 2). [score:5]
The 6-carboxyl fluorescein (FAM)-labeled miR-214 mimics, miR-214 inhibitors, mimic negative control (NC), inhibitor NC, Mfn2 siRNA and blank plasmid dry powder (Shanghai Gene Pharmaceutical Technology Corporation, Shanghai, China) underwent transient centrifugation and were dissolved in ddH [2]O containing diethylpyrocarbonate (DEPC). [score:5]
Those results indicate that the suppression of miR-214 is able to promote the EMT process and further lead to IC by up -regulating Mfn2. [score:4]
11, 25 Moreover, several studies have also demonstrated that the down-regulation of miR-214 can be used to determine the diagnosis, progression and recurrence of bladder cancer. [score:4]
In our study, the dual luciferase reporter suggested that, which is consistent with the results reflected in the study by Bucha et al., [27] who reported that miR-214 can regulate mitochondrial morphology and the cell cycle by targeting Mfn2. [score:4]
Additionally, in accordance with our finding, Sun et al. [28] identified Mfn2 as a direct target gene of miR-214. [score:4]
Compared with the blank group, miR-214 expression increased, but Mfn2 mRNA expression decreased in the miR-214 mimics and Mfn2 siRNA groups. [score:4]
Compared with the Mfn2-3′-UTR-WT+miR-214 mimics group, Y/H significantly increased in the Mfn2-3′-UTR-WT+miR-214 inhibitors, Mfn2-3′-UTR-MUT+miR-214 mimics and Mfn2-3′-UTR-MUT+miR-214 inhibitors groups (all P<0.05). [score:4]
Therefore, our study aims to explore the roles miR-214 plays in the ADMSC epithelial mesenchymal transition (EMT) process and the development of IC in postmenopausal women by targeting Mfn2. [score:4]
One section underwent qRT-PCR to detect the miR-214 and Mfn2 mRNA expression levels. [score:3]
Mfn2 is the target gene of miR-214. [score:3]
Expression levels of miR-214, Mfn2 mRNA and EMT markers in the seven groups. [score:3]
There was no significant difference among the mimics NC, inhibitors NC, miR-214 mimics+Mfn2 siRNA, NS and blank groups (Figure 11). [score:3]
Further analysis suggests that miR-214 is able to target Mitofusin 2 (Mfn2) and mediate the fibrosis process. [score:3]
These results implied that Mfn2 was the target gene of miR-214 in IC. [score:3]
Expression levels of miR-214, Mfn2 mRNA and EMT markers in normal bladder tissues, normal bladder cells treated with exosomes and IC bladder tissues. [score:3]
The cells were subcultured at 1: 3. On the 10th day, the expression levels of miR-214 and Mfn2 mRNA were detected by quantitative real-time PCR (qRT–PCR). [score:3]
There was no significant difference among the mimics NC, inhibitors NC, miR-214 mimics+Mfn2 siRNA and blank groups (Figure 8). [score:3]
Our data suggest that miR-214 is inhibited and Mfn2 is elevated in IC bladder tissues and that. [score:3]
No significant difference was found among the mimics NC, inhibitors NC, miR-214 mimics+Mfn2 siRNA, NS and blank groups (Figure 10). [score:3]
In addition, the suppression of miR-214 is able to promote the EMT process and contribute to bladder wall fibrosis, thus leading to IC in postmenopausal women, which provides a novel insight into IC treatment. [score:3]
No significant difference was found among the mimics NC, inhibitors NC, miR-214 mimics+Mfn2 siRNA and blank groups (Figure 9). [score:3]
Compared with the blank group, the expression levels of E-cadherin and ZO-1 mRNA and protein decreased, whereas those of N-cadherin, Fibronectin, Twist1, Snail and Vimentin mRNA and protein increased in the miR-214 mimics and Mfn2 siRNA groups. [score:2]
It was found that a fragment of miR-214 nucleotide was complementary with Mfn2 at the 5′-UTR, which was a highly conserved sequence compared with the miR-214 series among many species, indicating that Mfn2 could be the target gene of miR-214 (Figure 6). [score:2]
The IHC staining results showed that compared with the blank group, Mfn2 expression significantly decreased in the miR-214 mimics and Mfn2 siRNA groups. [score:2]
[5] Recently, increasing evidence has demonstrated that miR-214 is involved in the development and progression of bladder cancer. [score:2]
[9] Therefore, we predicted that there may be an association between miR-214 and IC. [score:1]
9, 26 Therefore, we predicted that miR-214 may be involved in IC. [score:1]
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[+] score: 206
Other miRNAs from this paper: rno-mir-148b
OVX-ASCs were mock-transduced (transduced without BV, Mock group) or co-transduced with 2 recombinant BV BacECre (expressing Cre) and Bac214S (expressing 10 repeats of miR-214 sponge, Fig.   S1), which prolongs miR-214 sponge expression for > 14 days and downregulates miR-214 in OVX-BMSCs [12]. [score:10]
If TAB2 or CTNNB1 are targets of miR-214, high levels of miR-214 can bind to TAB2-wt or CTNNB1-wt and suppress the Fluc expression, but high levels of miR-214 would not bind to TAB2-mut or CTNNB1-mut to repress Fluc expression. [score:9]
In light of our data, we propose a mo del (Fig.   8) that OVX-ASCs express aberrantly high level of miR-214, which targets TAB2 and CTNNB1 and hence blocks the Wnt pathway, leading to the overexpression of PPAR-γ and C/EBP-α and preferential differentiation into adipocytes. [score:7]
BacECre transiently expressed Cre recombinase; BacLEBW expressed human bone morphogenetic protein 2 (BMP2) and Bac214S expressed d2EGFP with 10 tandem hsa-miR-214-3p binding sites (miR-214 sponge) at the 3′-UTR. [score:7]
OVX-ASCs were mock-transduced (Mock group), co-transduced with BacECre/BacLEBW (LEBW group for BMP2 expression), BacECre/Bac214S (214S group for miR-214 sponge expression) or BacECre/BacLEBW/Bac214S (LEBW/214S group for sustained BMP2/miR-214 sponge expression), loaded into gelatin scaffolds at 1 dpt, and implanted into the critical-size defects (3 mm in diameter) at the left femoral metaphysis of osteoporotic rats. [score:7]
It is possible that suppressing miR-214 concurrently elevates miR-148b and decreases noggin expression, thus enhancing bone repair by alleviating the negative regulation. [score:6]
Compared with the Sham-Mock (expressing low levels of miR-214) transfected with the same plasmids, transfection of OVX-Mock (expressing high levels of miR-214) with TAB2-wt (Fig.   2c) or CTNNB1-wt (Fig.   2d) significantly (p < 0.05) reduced the luciferase activity, but transfection of OVX-Mock and OVX-214S with TAB2-mut or CTNNB1-mut did not diminish the luciferase activity, indicating that miR-214 targeted TAB2 and CTNNB1 genes. [score:6]
However, suppressing miR-214 by the BV-expressed miR-214 sponge reprogrammed the differentiation preference. [score:5]
Recently, miR-214 was found to be highly expressed in bone specimen from aged osteoporotic patients with fractures [11], suggesting the correlation of miR-214 overexpression with poor bone repair in osteoporotic patients. [score:5]
Suppressing intracellular miR-214 in OVX-ASCs concomitantly decreased the exosomal miR-214 secretion, thereby alleviating the inhibitory effects and promoting bone repair. [score:5]
Consequently, miR-214 overexpression in OVX-ASCs suppressed β-catenin and TAB2, resulting in the blockade of Wnt signaling and impaired osteogenesis potential. [score:5]
Orso F miR-214 and miR-148b targeting inhibits dissemination of melanoma and breast cancerCancer Res. [score:5]
We also uncovered aberrant miR-214 overexpression in BMSCs isolated from ovariectomized (OVX) rats (OVX-BMSCs), and suppressing miR-214 with miR-214 sponge (RNA that contains complementary binding sites to miR-214) promotes OVX-BMSCs osteogenesis and augments the ability of OVX-BMSCs to heal critical-size bone defects in osteoporotic rats [12]. [score:5]
miR-214 targeted TAB2 and CTNNB1 in the Wnt pathway to regulate OVX-ASCs differentiation. [score:4]
Compared with the Sham group, the Mock group (expressing abundant miR-214) expressed significantly less (p < 0.05) active β-catenin/Runx2, but more C/EBP-α. [score:4]
Nonetheless, by using the hybrid BV persistently expressing miR-214 sponge (214S group), we were able to knockdown miR-214 in OVX-ASCs to a level similar to that in Sham-ASCs, hence reversed the adipogenic/osteogenic differentiation bias and enhanced OVX-ASCs osteogenesis (Fig.   1). [score:4]
Therefore, suppressing miR-214 regulated osteogenesis/adipogenesis via the Wnt pathway. [score:4]
We further exploited the Cre/loxP -based BV persistently expressing miR-214 sponge to engineer OVX-ASCs, so as to knockdown intracellular and exosomal miR-214 levels, reverse the differentiation preference, substantiate osteogenesis and ameliorate bone healing in OVX rats. [score:4]
These data demonstrated that co -expressing BMP2/miR-214 sponge in OVX-ASCs exerted synergistic bone healing effects when compared with expressing miR-214 sponge alone. [score:4]
Despite the difficulty to repair osteoporotic bone defects, implanting OVX-ASCs whose intracellular miR-214 level was knocked down by BV-expressed miR-214 sponge (214S group) remarkably repaired the bone defects in 5 weeks (Figs  5– 7). [score:4]
The alleviated exosomal miR-214-triggered inhibition and enhanced BMP7 -mediated stimulation contributed to the enhanced osteogenesis of co-cultured OVX-BMSCs. [score:3]
Using OVX rats as the osteoporotic animal mo del, we found that OVX-ASCs highly expressed miR-214 and exhibited impaired osteogenesis capability but favored adipogenic differentiation (Fig.   1). [score:3]
Very recently it was reported that exosomal miR-214 secreted by osteoclast can be transferred to osteoblasts to inhibit osteoblastic activity [38]. [score:3]
Figure  4a delineates that the Mock group (highly expressed miR-214) secreted more (p < 0.05) exosomal miR-214 than the Sham-group. [score:3]
These data altogether demonstrated that OVX-ASCs co -expressing BMP2 and miR-214 sponges revived the bone microarchitecture in osteoporotic rats. [score:3]
[12]), BacECre/Bac214S (214 S group) or BacECre/BacLEBW/Bac214S (LEBW/214 S group for sustained BMP2/miR-214 sponge expression), loaded into gelatin scaffolds at 1 dpt, and implanted into the defects (n = 8 for each group at week 5 (5W); n = 4 for each group at week 2 (2W)). [score:3]
Figure 3Suppressing miR-214 in OVX-ASCs stimulated the osteogenesis of co-cultured OVX-BMSCs. [score:3]
To explore whether OVX-ASCs favored adipogenic differentiation and the role of miR-214 overexpression, OVX-ASCs (Mock and 214 S groups) and Sham-ASCs (Sham group) were cultured in osteoinduction or adipoinduction medium and analyzed by qRT-PCR. [score:3]
However, the 214 S group released significantly lower levels of exosomal miR-214, indicating that suppressing intracellular miR-214 concomitantly repressed the secretion of exosomal miR-214. [score:3]
Suppressing miR-214 in OVX-ASCs altered exosomal miR-214 and cytokine secretion. [score:3]
The potential miR-214-3p binding sequences at the 3′-UTR of TAB2 and CTNNB1 were predicted using the TargetScan 6.2 and microRNA. [score:3]
miR-214 also targets osterix [27] and ATF4 [28] that dictate the differentiation into mature osteoblasts and to osteocytes, respectively, thereby further repressing osteogenesis. [score:3]
Consequently, suppressing miR-214 activates Wnt pathway, which not only blocks PPAR-γ/CEBP-α to mitigate adipogenesis but also enhances Runx2 levels, de-represses osterix and ATF4, hence additively promoting the osteogenic differentiation of OVX-ASCs. [score:3]
These data collectively confirmed that OVX-ASCs aberrantly overexpressed miR-214 and favorably committed to adipogenic rather than osteogenic lineage, but alleviating miR-214 level switched the differentiation from adipogenic towards osteogenic lineage. [score:3]
Figure 4Suppressing miR-214 in OVX-ASCs altered exosomal miR-214 and cytokine secretion. [score:3]
miR-214 was recently found to target baculoviral IAP repeat-containing 7 in human osteoblasts [26], Osx in C2C2 cells [27] and ATF4 (another TF important for osteogenic differentiation) in mouse OVX-BMSCs [28]. [score:3]
First, suppressing miR-214 reprogramed the propensity of OVX-ASCs differentiation from adipogenic to osteogenic by reviving the Wnt signaling mediator β-actin/TAB2 (Figs  1 and 2). [score:3]
These mechanisms converge to improve the commitment of miR-214 sponge -expressing OVX-ASCs towards osteogenic lineage and augment bone healing in OVX rats via autocrine and paracrine effects. [score:3]
BMP2/miR-214 sponge co -expression further synergizes the OVX-ASCs osteogenesis and bone healing in OVX rats. [score:3]
By co -expressing BMP2 and miR214 sponge in the OVX-ASCs, the LEBW/214S group further substantiated the bone regeneration, as evidenced by the complete defect filling, improved cortical bone structure (Figs  4 and 5), highest BV/TV, BMD, Tb. [score:3]
Nonetheless, reducing miR-214 levels in OVX-ASCs (214 S group) raised the levels of active β-catenin/Runx2 and repressed the C/EBP-α expression (Fig.   2e,f). [score:3]
Suppressing miR-214 in OVX-ASCs stimulated the osteogenesis of co-cultured OVX-BMSCs. [score:3]
qRT-PCR analysis (Fig.   1a) revealed ≈3.5 fold miR-214 expression in mock-transduced OVX-ASCs (Mock) as opposed to Sham-ASCs. [score:3]
Here we unraveled two new miR-214 targets: CTNNB1 (β-catenin) and TAB2 (Fig.   2). [score:3]
miR-214 regulates the switching of adipogenesis and osteogenesis in OVX-ASCs. [score:2]
To dissect how miR-214 regulated the adipogenesis/osteogenesis switching, we performed bioinformatic prediction, which revealed high complementarity between miR-214 and the 3′-UTR of TAB2 and CTNNB1 genes. [score:2]
Additionally, we uncovered that knocking down miR-214 levels in OVX-ASCs (214S group) stimulated the osteogenesis of co-cultured OVX-BMSCs via a paracrine manner (Fig.   3), which was accompanied by reduced release of exosomal miR-214 and OPN as well as increased secretion of BMP7 and OPG (Fig.   4). [score:2]
Meanwhile, knocking down miR-214 levels in OVX-ASCs enhances BMP7/OPG secretion and lowers exosomal miR-214/OPN secretion, which simultaneously enhances the osteogenesis of host OVX-BMSCs and attenuates the host osteoclast activity. [score:2]
Likewise, co-transduction of OVX-ASCs with BacECre/Bac214S (214 S group) knocked down the endogenous miR-214 to a level statistically similar (p > 0.05) to that in Sham-ASCs (Fig.   1a). [score:2]
Therefore, we mock-transduced OVX-ASCs (Mock group) or co-transduced OVX-ASCs (214 S group) as in Fig.   1, isolated exosomes at 3 dpt from the supernatant and analyzed the exosomal miR-214 by qRT-PCR. [score:1]
To elucidate whether miR-214 blocked the Wnt pathway, cells in the Mock, 214 S and Sham groups were analyzed at 3 dpt by (Fig.   2e) and densitometry (Fig.   2f). [score:1]
Figure 8 A mo del accounting for how miR-214 orchestrates osteogenesis and adipogenesis in OVX-ASCs. [score:1]
In conclusion, this study implicates the potential of engineering osteoporotic ASCs by repressing miR-214 as a means to treat osteoporotic fractures. [score:1]
These data shed light on how miR-214 functions as a “molecular switch” controlling the OVX-ASCs differentiation, and provided new insights into why repressing miR-214 levels can shift the OVX-ASCs differentiation from adipogenic to osteogenic. [score:1]
High miR-214 levels in OVX-ASCs also increases exosomal miR-214/OPN secretion but decreases BMP7/OPG secretion, which concurs with compromised osteogenesis of co-cultured OVX-BMSC. [score:1]
Quantitative real-time reverse-transcription PCR (qRT-PCR) and miR-214 analysis. [score:1]
We mock-transduced OVX-ASCs (Mock group) or co-transduced OVX-ASCs (214S group) as in Fig.   1, isolated extracellular exosomes at 3 dpt and analyzed the exosomal miR-214 by qRT-PCR. [score:1]
Furthermore, miR-214 and miR-148b antagonize the effects of each other in cancer cells [42]. [score:1]
Mature miRNAs in the cells were isolated using Trizol (Invitrogen) while miR-214 in the exosomes were isolated using miRCURY™ Exosome Isolation Kit (Exiqon), followed by miRNA extraction using Trizol. [score:1]
Using ASCs isolated from OVX rats (OVX-ASCs), here we investigated the miR-214 expression level, adipogenesis/osteogenesis preference, molecular pathway and how miR-214 affects the differentiation of surrounding OVX-BMSCs in vitro and bone healing in OVX rats. [score:1]
Third, exosomal miR-214 undermines in vivo bone formation [38]. [score:1]
Exosomal miR-214 from Sham-ASCs were analyzed in the same manner. [score:1]
To examine the miR-214 levels in osteoporotic ASCs, we first created osteoporotic rat mo dels by ovariectomy (OVX). [score:1]
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[+] score: 166
As for the signaling pathway, the miR-214 not only could suppress the upstream signaling molecule RAS in MAPK pathways [17], it might directly suppress the expression of JNK and ERK [31, 32]. [score:8]
a Decreased miR-214 expression in Jurkat cells after transfection with miR-214 inhibitor versus scramble oligonucleotides; (b) in Jurkat cells transfected miR-214 inhibitor or controls, the apoptotic rate was increased after cultured with TNF-α (20 ng/mL) for 24 h compared with those cultured with medium alone. [score:6]
Among the nine T-cell miRNAs affected by TNF-α and downregulated in RA T cells, the expression levels of miR-139-3p, miR-204, miR-214, and miR-760 were increased in patients using biologic agents. [score:6]
First, we successfully transfected miR-214 inhibitor into Jurkat cells and the expression levels of miR-214 were modest but significantly lower in Jurkat cells transfected with miR-214 inhibitor compared with the controls (Fig.   3a). [score:6]
Tian X Zeng G Li X Wu Z Wang L Cantharidin inhibits cell proliferation and promotes apoptosis in tongue squamous cell carcinoma through suppression of miR-214 and regulation of p53 and Bcl-2/BaxOncol Rep. [score:6]
Each scatter spot representing average normalized expression level of miRNA in three repeats of each treatment; (b) 13 miRNAs exhibiting aberrant expression in Jurkat cells cultured with TNF-α (20 ng/mL) for 7 days; (c) decreased expression of miR-139-3p, miR-204, miR-760, miR-524-5p, miR-136, miR-548d-3p, miR-214, miR-383, and miR-887 in RA T cells miRNA, compared with normal T cells. [score:6]
Among various systemic autoimmune diseases, decreased expression of miR-214 was found in patients with multiple sclerosis [33]. [score:5]
It has been reported that miR-214 could inhibit the protein expression of Ras [19], an upstream activator of ERK and JNK. [score:5]
The expression levels of 12 miRNAs, including miR-139-3p, miR-204, miR-760, miR-432, miR-524-5p, miR-136, miR-548d-3p, miR-206, miR-214, miR-383, miR-224, and miR-887 were significantly lower, whereas the expression level of miR-146a was significantly higher, in Jurkat cells after being cultured with TNF-α for 7 days (fold change > 4, p < 0.05, Fig.   1b). [score:5]
Jindra PT Bagley J Godwin JG Iacomini J Costimulation -dependent expression of microRNA-214 increases the ability of T cells to proliferate by targeting PtenJ Immunol. [score:5]
Huang HJ Liu J Hua H Li SE Zhao J Yue S MiR-214 and N-ras regulatory loop suppresses rhabdomyosarcoma cell growth and xenograft tumorigenesisOncotarget. [score:5]
Initially, our studies showed that among the expression of T cell miRNAs affected by TNF-α in Jurkat cells, the expression levels of miR-139-3p, miR-204, miR-760, miR-383, miR-524-5p, miR-136, miR-548d-3p, and miR-214 were significantly decreased in RA T cells. [score:5]
It has been found that increased expression of miR-214 in T cells upon activation [34] and increased miR-214 expression could promote the release of inflammatory cytokines, such as TNF-α and interleukin (IL)-6 in murine macrophages [35]. [score:5]
Zhang ZC Li YY Wang HY Fu S Wang XP Zeng MS Knockdown of miR-214 promotes apoptosis and inhibits cell proliferation in nasopharyngeal carcinomaPLoS One. [score:4]
Expression levels of miR-139-3p, miR-204, miR-214, and miR-760 were correlated with the use of biologic agents. [score:3]
The transfection of miR-214 mimic suppressed TNF-α -mediated apoptosis of Jurkat cells. [score:3]
We speculated that the decreased expression of miR-214 might contribute to the activation of ERK and JNK. [score:3]
The apoptotic rate was similar in Jurkat cells transfected with miR-214 mimic cultured either in the presence or absence of TNF-α (Fig.  2c) Fig. 3Effects of miR-214 inhibitor (miR-214i) transfection in Jurkat cells apoptosis. [score:3]
The expression levels of miR-139-3p, miR-204, miR-214, and miR-760 increased in RA patients receiving biologic agents. [score:3]
The transfection of miR-214 reversed the TNF-α -mediated cells apoptosis and inhibited the phosphorylation of ERK and JNK in Jurkat cells. [score:3]
The relative expression level of miRNA was defined as (39 – Ct) after adjusting with an internal control (U6 small nuclear RNA) Fig. 2Effects of miR-214 mimic transfection in Jurkat cells apoptosis. [score:3]
Jurkat cells were transfected with miR-214 mimic, miR-214 inhibitor or scramble oligonucleotides (all from Ambion, Austin, TX, USA) using the conditions previously described [16], and then cultured with TNF-α (20 ng/mL) at 37 °C for 24 h or 48 h for further analysis of cell apoptosis or Western blot analysis, respectively. [score:3]
The expression levels of miR-214 showed a significant correlation with the serum CRP levels and the use of biologic agents. [score:3]
Transfection of miR-214 inhibitor did not affect survival of Jurkat cells. [score:3]
Transfection of miR-214 mimic suppressed TNF-α -mediated apoptosis of Jurkat cells. [score:3]
Since the expression levels of miR-214 were statistically significant correlated with the serum CRP levels and the use of biologic agents. [score:3]
Transfection of Jurkat cells with miR-214 mimic suppressed both the basal and TNF-α -mediated ERK and JNK phosphoryation. [score:3]
The expression levels of miR-139-3p, miR-204, miR-214, and miR-760 increased in RA patients using biologic agents. [score:3]
Decreased expression of miR-139-3p, miR-204, miR-760, miR-524-5p, miR-136, miR-548d-3p, miR-214, miR-383, and miR-887 were noted in RA T cells. [score:3]
Whether cultured with TNF-α or not, the apoptotic rate of Jurkat cells was not different between those transfected with miR-214 inhibitors and the controls Fig. 4Comparison of ERK and JNK protein phosphorylation in T-cell lysates from RA and control groups as detected by Western blot analysis. [score:3]
Then, we transfected miR-214 inhibitor and controls into Jurkat cells and cultured in the presence or absence of TNF-α for 24 hours. [score:3]
Therefore, the pathologic role of decreased expression of miR-214 in T cells from patients with RA might be an insufficient negative feedback to stop the inflammatory response similar to the role of miR-146a in the immunopathogenesis of RA [5]. [score:3]
The apoptotic rates of Jurkat cells were both significantly elevated in Jurkat cells transfected with miR-214 inhibitor and controls. [score:3]
Wang F Liu M Li X Tang H MiR-214 reduces cell survival and enhances cisplatin -induced cytotoxicity via down-regulation of Bcl2l2 in cervical cancer cellsFEBS Lett. [score:3]
We found that miR-214 could suppress both the basal level and TNF-α -induced ERK and JNK phosphorylation and apoptosis in Jurkat cells. [score:3]
Increased (a) ERK and (b) JNK phosphorylation in nine patients with RA and six healthy controls, normalized to actin expression; (c) ERK and JNK protein phosphorylation in T cell lysates of three patients with RA and two healthy controls as representative tests Fig. 5Effect of miR-214 on ERK and JNK protein phosphorylation in Jurkat cells. [score:3]
Moreover, RA patients with each 1 mg/dL increment of CRP levels had a significant 0.65-fold decrease (p = 0.025; 95% CI 0.45–0.94) and the use of biologic agents had a significant 2.44-fold increase (p = 0.032; 95% CI 1.08–5.48) in miR-214 expression levels. [score:3]
Zhao L Liu YW Yang T Gan L Yang N Dai SS The mutual regulation between miR-214 and A2AR signaling plays an important role in inflammatory responseCell Signal. [score:2]
The impact of dysregulated miR-214 for cell apoptosis is still controversial [27– 30]. [score:2]
The fold changes of expression levels for these miRNAs were 0.42-fold for miR-139-3p, 0.43-fold for miR-204, 0.13-fold for miR-760, 0.32-fold for miR-524-5p, 0.45-fold for miR-136, 0.19-fold for miR-548d-3p, 0.37-fold for miR-214;0.36-fold for miR-383, and 0.14-fold for miR-887, compared with controls. [score:2]
The expression of miR-139-3p, miR-204, miR-760, miR-524-5p, miR-136, miR-548d-3p, miR-214, miR-383, and miR-887 was found to be significantly lower in RA T cells (p < 0.05), compared with controls (Fig.   1c). [score:2]
e In Jurkat cells after transfection with miR-214 mimic or scramble oligonucleotides cultured with TNF-α (20 ng/mL) for 48 h, the phosphorylation ratio of ERK and JNK decreased in those transfected with miR-214 mimic compared with the control groups and (f) a representative case Expression profiles of 270 miRNAs in Jurkat cells cultured in the presence or absence of TNF-α (20 ng/mL) for 7 days are displayed in Fig.   1a, with each scatter spot represents the average of three adjusted miRNA levels from each group. [score:2]
Whether cultured in the presence or absence of TNF-α, there were no significant differences in the apoptotic rates of Jurkat cells transfected with miR-214 inhibitor compared with the controls (Fig.   3b). [score:2]
We further surveyed the functional effects of miR-214 in T cells. [score:1]
Transfection of miR-214 into Jurkat cells. [score:1]
a Remarkable elevation of miR-214 expression levels in Jurkat cells after transfection with miR-214 mimic versus controls (transfected with scramble oligonucleotides); (b) increased Jurkat cells apoptosis after cultured with TNF-α (20 ng/mL) for 7 days, compared with culture medium alone; (c) in Jurkat cells transfected scrambled oligonucleotides, the apoptotic rate of Jurkat cells was increased after cultured with TNF-α (20 ng/mL) for 24 h compared with those cultured with medium alone. [score:1]
The transfection of miR-214 mimic reversed the TNF-α mediated cell apoptosis as well as ERK and JNK phosphorylation and thus appeared to be involved in the immunopathogenesis of RA. [score:1]
In contrast, the apoptotic rate was similar in Jurkat cells transfected with miR-214 mimic after cultured in the presence or absence of TNF-α (Fig.   2c). [score:1]
Then, we transfected miR-214 mimic and controls into Jurkat cells and cultured them in the presence or absence of TNF-α for 24 hours. [score:1]
Since the expression levels of miR-214 were significantly correlated with the serum CRP levels and the use of biologic agents, we further investigated the functional effects of miR-214 in T cells. [score:1]
First, we successfully transfected miR-214 mimic into Jurkat cells (Fig.   2a). [score:1]
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Our data showed that miR-214 inhibits Bax expression increased propotionally with 2BD or 3BD construct (Fig. 4A), thus confirming that miR-214 targeted Bax and downregulated its expression. [score:12]
miR-214 targets Bax 3′UTR and downregulates Bax expression by inhibiting its mRNA translation. [score:12]
Our data showed that the relative number of EGFP positive cells in RFP positive cells was decreased in the miR-214 and mimic miR-214 transfected groups, but not in the scramble, miR-214 inhibitor or mutant miR-214 groups (Fig. 3D), suggesting that miR-214 downregulated Bax expression. [score:8]
In addition to Bax expression that may be regulated by miR-214, one single nucleotide polymophism (SNP) in presenilin-1 (PS1) (rs63750082) was shown to create a potential target site for miR-214 [45]. [score:6]
Our data showed that cell death was significantly inhibited by miR-214 or mimic miR-214 injection, and enhanced by miR-214 inhibitor injection (Fig. 4F). [score:5]
For experiments described in Fig. 3, human miR-214, scramble microRNA control, mimic miR-214, miR-214 inhibitor and mutant miR-214 (5′-ACAG ACGGCACAGACAGGCAGU-3′), and for experiments described in Fig. 4F–I, rat miR-214, scramble microRNA control, mimic miR-214, miR-214 inhibitor were all purchased from Qiagen (Hilden, Germany). [score:5]
Therefore, isoflurane enhanced Aβ cytotoxicity through downregulating miR-214. [score:4]
Isoflurane Increased Bax Level through Downregulating miR-214. [score:4]
To this end, we transfected the neuroblastoma SH-Sy5y cells with human Bax 3′UTR regulated EGFP construct and co -transfected with control, scramble microRNA, miR-214, mimic miR-214, miR-214 inhibitor or mutant miR-214, respectively. [score:4]
Among the microRNAs altered by isoflurane application, miR-214 was significantly downregulated (Fig. 3B). [score:4]
These data together indicate that miR-214 regulated Bax mRNA translation. [score:4]
This may result in the downregulation of PS1 by miR-214 and thereby reduces the production of Aβ and lessens AD pathology. [score:4]
Therefore, isoflurane induces cytotoxicity and neuronal cell death in the presence of Aβ through downregulating miR-214 (Fig. 5). [score:4]
Time course of miR-214 indicated that maximal inhibition happened at 12–24 hours after transfection, although the effect might last for at least 48 hours (Fig. 3F). [score:3]
There are no significant correlation between miR-214 expression and age (R [2] = −0.69457) or postmortem intervals (R [2] = −0.39699) (Fig. 4E). [score:3]
We found that isoflurane decreased the level of miR-214, which inhibited Bax activation. [score:3]
In accord with the notion that miR-214 level may be releated to Bax abundance, Bax 3′UTR was predicted to be a target of miR-214 (Fig. 3A). [score:3]
Neurons were microinjected with miR-214, mimic miR-214, miR-214 inhibitor or scramble sequence and insulted with eAβ [1-42]. [score:3]
Our data indicate that miR-214 can reverse isoflurane -induced cell death in the presence of eAβ [1-42], which can be mimicked by Bax suppression. [score:3]
M-miR-214: mimic miR-214; I-miR-214: miR-214 inhibitor. [score:3]
QIAgen Miscript SYBR Green PCR kit (cat # 218073) was used to detect miR-214 expression. [score:3]
Similarly, Bax 3′UTR regulated luciferase assay showed miR-214 from 20 to 100 nM efficiently decreased Bax expression (Fig. 3E). [score:3]
When mutant Bax 3′UTR was co -transfected into SH-Sy5y cells with either scramble or miR-214 sequence, luciferase reportor assay showed no significant difference between scramble and miR-214 transfected groups (Fig. 4A), suggesting that miR-214 targeted Bax 3′UTR specifically. [score:2]
Isoflurane regulated cell death through miR-214. [score:2]
To further confirm the role of miR-214 in regulating Bax level, mutant Bax 3′UTR was made by altering 2 nucleotides at WT Bax 3′UTR region. [score:2]
To further proof that miR-214 regulate Bax 3′UTR selectively, microtubule -associated protein 2 (MAP2) 3′UTR was co -transfected with scramble or miR-214 sequence. [score:2]
However, our results in the postmortem hippocampal tissues from 8 matched control-AD pairs indicate that there is no discernible change in the miR-214 level in AD. [score:1]
0055276.g004 Figure 4(A) miR-214 specifically acted on Bax 3′UTR. [score:1]
Similarly, the cell death induced by isoflurane with iAβ [1-42] and the combination of serum deprivation and Aβ can also be reversed by miR-214 (Fig. 4G–I), suggesting that miR-214 is indeed involved in isoflurane cytotoxicity. [score:1]
Together with our data indicating that isoflurane reduces miR-214 to increase cell death by promoting Aβ [1-42] cytotoxicity, there data support the idea that inhaled anesthetics may increase the risk of AD [33]. [score:1]
Most importantly, our finding in this study suggests that therapies that increase miR-214 may be used to reduce the neurotoxicity and post-operative cognitive dsyfunction following the usage of inhaled anesthetics, especially in AD patients. [score:1]
The RT-PCR results of hippocampal tissues from 8 matched control-AD pairs with miR-214 showed that there was no discernible difference detected between two diagnostic groups (p = 0.38281, two-tailed Student’s t-test). [score:1]
0055276.g003 Figure 3(A) Sequence alignment of human and rat miR-214 and Bax 3′UTR. [score:1]
Our data prove no noticeable different between scramble and miR-214 groups (Fig. 4A). [score:1]
To assess whether AD affects the level of miR-214, we measured miR-214 expression in the postmortem tissues from AD patients or age matched controls. [score:1]
Isoflurane decreased miR-214. [score:1]
Our data indicated that following anesthetic treatment, miR-214 level was decreased significantly in both brain tissues and CSF (Fig. 4D). [score:1]
RT-PCR results for hippocampal tissues from 8 matched control-AD pairs with miR-214 showed that there was no discernible difference detected between two diagnostic groups (p = 0.38281, two-tailed Student’s t-test). [score:1]
We then verified the effect of miR-214 on cell death in rat primary neurons. [score:1]
Western blot data showed that in SH-Sy5y cells, miR-214 and mimic miR-214 decreased Bax level (Fig. 4B), while Bax mRNA levels were not altered by miR-214 (Fig. 4C). [score:1]
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[+] score: 104
Other miRNAs from this paper: mmu-mir-30a, mmu-mir-101a, mmu-mir-125a, mmu-mir-125b-2, mmu-mir-132, mmu-mir-134, mmu-mir-135a-1, mmu-mir-138-2, mmu-mir-142a, mmu-mir-150, mmu-mir-154, mmu-mir-182, mmu-mir-183, mmu-mir-24-1, mmu-mir-194-1, mmu-mir-200b, mmu-mir-122, mmu-mir-296, mmu-mir-21a, mmu-mir-27a, mmu-mir-92a-2, mmu-mir-96, rno-mir-322-1, mmu-mir-322, rno-mir-330, mmu-mir-330, rno-mir-339, mmu-mir-339, rno-mir-342, mmu-mir-342, rno-mir-135b, mmu-mir-135b, mmu-mir-19a, mmu-mir-100, mmu-mir-139, mmu-mir-212, mmu-mir-181a-1, mmu-mir-214, mmu-mir-224, mmu-mir-135a-2, mmu-mir-92a-1, mmu-mir-138-1, mmu-mir-181b-1, mmu-mir-125b-1, mmu-mir-194-2, mmu-mir-377, mmu-mir-383, mmu-mir-181b-2, rno-mir-19a, rno-mir-21, rno-mir-24-1, rno-mir-27a, rno-mir-30a, rno-mir-92a-1, rno-mir-92a-2, rno-mir-96, rno-mir-100, rno-mir-101a, rno-mir-122, rno-mir-125a, rno-mir-125b-1, rno-mir-125b-2, rno-mir-132, rno-mir-134, rno-mir-135a, rno-mir-138-2, rno-mir-138-1, rno-mir-139, rno-mir-142, rno-mir-150, rno-mir-154, rno-mir-181b-1, rno-mir-181b-2, rno-mir-183, rno-mir-194-1, rno-mir-194-2, rno-mir-200b, rno-mir-212, rno-mir-181a-1, rno-mir-296, mmu-mir-376b, mmu-mir-370, mmu-mir-433, rno-mir-433, mmu-mir-466a, rno-mir-383, rno-mir-224, mmu-mir-483, rno-mir-483, rno-mir-370, rno-mir-377, mmu-mir-542, rno-mir-542-1, mmu-mir-494, mmu-mir-20b, mmu-mir-503, rno-mir-494, rno-mir-376b, rno-mir-20b, rno-mir-503-1, mmu-mir-1224, mmu-mir-551b, mmu-mir-672, mmu-mir-455, mmu-mir-490, mmu-mir-466b-1, mmu-mir-466b-2, mmu-mir-466b-3, mmu-mir-466c-1, mmu-mir-466e, mmu-mir-466f-1, mmu-mir-466f-2, mmu-mir-466f-3, mmu-mir-466g, mmu-mir-466h, mmu-mir-504, mmu-mir-466d, mmu-mir-872, mmu-mir-877, rno-mir-466b-1, rno-mir-466b-2, rno-mir-466c, rno-mir-872, rno-mir-877, rno-mir-182, rno-mir-455, rno-mir-672, mmu-mir-466l, mmu-mir-466i, mmu-mir-466f-4, mmu-mir-466k, mmu-mir-466j, rno-mir-551b, rno-mir-490, rno-mir-1224, rno-mir-504, mmu-mir-466m, mmu-mir-466o, mmu-mir-466c-2, mmu-mir-466b-4, mmu-mir-466b-5, mmu-mir-466b-6, mmu-mir-466b-7, mmu-mir-466p, mmu-mir-466n, mmu-mir-466b-8, rno-mir-466d, mmu-mir-466q, mmu-mir-21b, mmu-mir-21c, mmu-mir-142b, mmu-mir-466c-3, rno-mir-322-2, rno-mir-503-2, rno-mir-466b-3, rno-mir-466b-4, rno-mir-542-2, rno-mir-542-3
ACTH up-regulated the expression of miRNA-212, miRNA-182, miRNA-183, miRNA-132, and miRNA-96 and down-regulated the levels of miRNA-466b, miRNA-214, miRNA-503, and miRNA-27a. [score:9]
Real-time PCR (qRT-PCR) measurements demonstrated that ACTH treatment upregulated the expression of miRNA-212, miRNA-183, miRNA-182, miRNA-132 and miRNA-96, while down -regulating the expression of miRNA-466b, miRNA-214, miRNA-503 and miRNA-27a. [score:7]
Real-time quantitative PCR measurements confirmed that the expression of miR-212, miRNA-183, miRNA-182, miRNA-132, miRNA-370, miRNA-377 and miRNA-96 was up-regulated and that of miRNA-122, miRNA-200b, miRNA-466b, miRNA-138, miRNA-214, miRNA-503 and miRNA-27a down-regulated in adrenals from 17α-E2 treated rats. [score:7]
The levels of miR-212, miRNA-183, miRNA-182, miRNA-132, miRNA-370, miRNA-377, and miRNA-96 were up-regulated, whereas miR-125b, miRNA-200b, miR-122, miRNA-466b, miR-138, miRNA-214, miRNA-503 and miRNA27a were down-regulated in response to 17α-E2 treatment. [score:7]
qRT-PCR measurements confirmed that the expression of miR-212, miRNA-183, miRNA-182, miRNA-132, miRNA-370, miRNA-377 and miRNA-96 was up-regulated and that of miRNA-122, miRNA-200b, miRNA-466b, miRNA-138, miRNA-214, miRNA-503 and miRNA-27a down-regulated in adrenals from 17α-E2 treated rats (Fig. 3 ). [score:7]
0078040.g006 Figure 6miRNA-132 and miRNA-214 binding sites in the 3′ UTR of the mouse SREBP-1c and LDLR genes mediate the downregulation of SREBP-1c and LDLR expression by miRNA-132 and miRNA-214, respectively. [score:6]
miRNA-132 and miRNA-214 binding sites in the 3′ UTR of the mouse SREBP-1c and LDLR genes mediate the downregulation of SREBP-1c and LDLR expression by miRNA-132 and miRNA-214, respectively. [score:6]
Bt [2]cAMP stimulation of granulosa cells caused down-regulation of a majority of miRNAs, including miRNA-200b, miRNA-466b, miRNA-27a, miRNA-214, miRNA-138 and miRNA-19a, but expression levels of miRNA-212, miRNA-183, miRNA-182, and miRNA-132 were significantly increased. [score:6]
We also obtained evidence that miR-132 and miRNA-214 inhibit the expression of SREBP-1c and LDLR, respectively. [score:5]
Significant expression was also observed for miRNA-27a, miRNA-132 and miRNA-214, whereas very low expression was noted for all of the remaining (seven) miRNAs. [score:5]
miRNA-132 and miRNA-214 Suppress SREBP-1c and LDLR by Targeting Specific Site(s) within the 3′ UTR of SREBP-1c and LDLR, Respectively. [score:5]
qRT-PCR measurements indicated that exposure of primary rat granulosa cells to Bt [2]cAMP for 24 h inhibited the expression of miRNA-200b, miRNA-466b, miRNA-27a, miRNA-214, and miRNA-138 and miRNA-19a while enhancing the expression of miRNA-212, miRNA-183, miRNA-182, and miRNA-132 (Fig. 4 ). [score:5]
Significant ACTH -induced down-regulation of miRNA-466b, miRNA-214, miRNA-503 and miRNA-27a was also observed (Fig. 3 ). [score:4]
Here, we directly assessed the binding of miRNA-138, miRNA-132 and miRNA-182/miRNA-214 to the 3′UTR of StAR, SREBP-1c, and LDLR, respectively, and regulation of their expression levels, by carrying out luciferase reporter gene assays. [score:4]
More specifically, we assessed the impact of Bt [2]cAMP treatment on the expression of miRNA-212, miRNA-122, miRNA-27a, miRNA-466b, miRNA-200b, miRNA-138, miRNA-214, miRNA-183, miRNA-182, miRNA-132, miRNA-96 and miRNA-19a. [score:3]
Overexpression of pre-miRNA-132 and pre-miRNA-214 significantly decreased the luciferase activity of the 3′UTR of the SREBP-1c and LDLR reporter containing micRNA-132 and miRNA-214 binding sites, respectively. [score:3]
The levels of expression of miRNA-212, miRNA-122, miRNA-138, miRNA-214, miRNA-183, miRNA-182, miRNA-132, miRNA-96, miRNA-466b, miRNA-200b, and miRNA-19a are shown. [score:3]
We next evaluated the effects of Bt [2]cAMP stimulation of rat ovarian granulosa cells and of mouse MLTC-1 Leydig tumor cells on the expression of twelve miRNAs (miRNA-212, miRNA-122, miRNA-183, miRNA-200b, miRNA-466b, miRNA-182, miRNA-96, miRNA-27a, miRNA-132, miRNA-214, miRNA-138 and miRNA-19a) whose adrenal expression was differentially altered in response to treatment of rats with ACTH, 17α-E2 or DEX. [score:3]
Overexpression of pre-miRNA-132 and pre-miRNA-214 significantly decreased the luciferase activity of the 3′UTR of the SREBP-1c and LDLR reporter containing micRNA-132 and miRNA-214 binding sites, respectively (Fig. 6 ). [score:3]
Quantitative RT-PCR (qRT-PCR) validation of miRNA-212, miRNA-200b, miRNA-183, miRNA-122, miRNA-19a, miRNA-466b, miRNA-182, miRNA-132, miRNA-138, miRNA-370, miRNA-96, miRNA-503, miRNA-27a and miRNA-214 levels in control, ACTH-, 17α-E2 or DEX -treated adrenals in vivo. [score:1]
CHO cells were co -transfected individually with StAR 3′-UTR (containing the putative site I or site II for miRNA-138 binding) ± pre-miRNA-138-5p (panel B), SREBP-1c 3′-UTR (containing the putative binding site for miRNA-132) ± pre-miRNA-132-3p, LDLR 3′-UTR (containing the putative binding site for miRNA-182), or LDLR 3′-UTR (containing the putative site I, site II or site III for miRNA-214 binding) ± pre-miRNA-214-3p for 36h, followed by determination of luciferase activities. [score:1]
Individual fragments of the 3′ UTR region of the StAR gene containing site I or site II binding site for miRNA-138-5p, the 3′-UTR of SREBP-1c containing a binding site for miRNA-132-5p, the 3′-UTR of LDLR containing a binding site for miRNA-182-5p or the 3′-UTR of LDLR containing site I, site II, or site III binding site for miRNA-214-3p were inserted downstream of the luciferase open reading frame of pMIR-REPORT vector. [score:1]
CHO cells were co -transfected individually with the StAR 3′-UTR (containing putative site I or site II for miRNA-138 binding) ± pre-miRNA-138-5p (panel B), the SREBP-1c 3′-UTR (containing putative binding site for miRNA-132) ± pre-miRNA-132-3p (panel C), the LDLR 3′-UTR (containing putative binding site for miRNA-182) (panel D), or the LDLR 3′-UTR (containing putative site I, site II or site III for miRNA-214 binding) ± pre-miRNA-214-3p for 36 h (panel E). [score:1]
0078040.g003 Figure 3Quantitative RT-PCR (qRT-PCR) validation of miRNA-212, miRNA-200b, miRNA-183, miRNA-122, miRNA-19a, miRNA-466b, miRNA-182, miRNA-132, miRNA-138, miRNA-370, miRNA-96, miRNA-503, miRNA-27a and miRNA-214 levels in control, ACTH-, 17α-E2 or DEX -treated adrenals in vivo. [score:1]
Seed sequences of the putative miRNA-138-5p, miRNA-132-3p and miRNA-182-5p/miRNA-214-3p binding sites in the 3′-UTR of mouse StAR, SREBP-1c and LDLR genes, respectively. [score:1]
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[+] score: 73
Among those seventeen deregulated miRNAs miR-31 was up-regulated on day 2, day 7 and day 14. miR-199a was up-regulated on day 7 and day 14. miR-214 was up-regulated on day 7 and day 14. miR-499 was down-regulated on day 2 and day 7. Table 1 miRNAs differentially expressed in the myocardial tissues of rats with acute myocardial infarction. [score:16]
Among those seventeen deregulated miRNAs miR-31 was up-regulated on day 2, day 7 and day 14. miR-199a was up-regulated on day 7 and day 14. miR-214 was up-regulated on day 7 and day 14. miR-499 was down-regulated on day 2 and day 7. Table 1 miRNAs differentially expressed in the myocardial tissues of rats with acute myocardial infarction. [score:16]
miRNA Host gene Function of host gene miR-923 UNC45B UNC45B plays a role in myoblast fusion and sarcomere organization miR-126 EGFL7 blood vessel development; angiogenesis; and vasculogenesis miR-26b CTDSP1 n/a miR-199a DNM2/DNM3 filopodium formation; centronuclear myopathy; growth and development of megakaryocytes miR-214 DNM3 filopodium formation; centronuclear myopathy; growth and development of megakaryocytes miR-499 MYH7B cardiac muscle, striated muscle contraction, striated muscle thick filament miRNA regulates gene expression by binding and modulating the translation of specific miRNAs. [score:9]
Expression levels of miR-126 and miR-499 were greatly down-regulated after AMI, whereas expression levels of miR-31 and miR-214 increased after AMI (Figure 3 and Additional File 4). [score:8]
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]
On day 14, miR-214, mir-923, miR-711, and miR-199a-3p, and miR-31 were up-regulated, of which miR-31 showed the most striking up-regulation (an increase of eight-fold compared with the sham-control). [score:6]
miRNA Host gene Function of host gene miR-923 UNC45B UNC45B plays a role in myoblast fusion and sarcomere organization miR-126 EGFL7 blood vessel development; angiogenesis; and vasculogenesis miR-26b CTDSP1 n/a miR-199a DNM2/DNM3 filopodium formation; centronuclear myopathy; growth and development of megakaryocytes miR-214 DNM3 filopodium formation; centronuclear myopathy; growth and development of megakaryocytes miR-499 MYH7B cardiac muscle, striated muscle contraction, striated muscle thick filament Microarray data mining and differential analyses resulted in 17 significantly deregulated miRNAs associated with AMI (Table 1, Figure 1). [score:5]
miRNA Tissues in which miRNA is most highly expressed tissueDay 2(Fold change/Q-value)Day 7(Fold change/Q-value)Day 14(Fold change/Q-value) miR-31 Colon4.504/0.000 [#]5.923/0.000 [#]8.224/0.000 [#] miR-18a Small intestine2.136/0.013 [#] 1.016/0.507 0.904/0.612 miR-18b Small intestine2.045/0.000 [#] 1.502/0.023 1.314/0.000 miR-214 Distal colon 1.970/0.0002.992/0.000 [#]2.404/0.000 [#] miR-223 Spleen4.063/0.013 [#] n/a n/a miR-923 n/a 1.461/0.160 n/a2.232/0.000 [#] miR-711 n/a n/a n/a2.542/0. [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: 69
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]
Since the down-regulation of microRNAs may cause the up-regulation of targeted genes, we hypothesized that the presence of IGF-1 triggers the expression of certain genes by down -regulating key microRNAs (miR-1224, miR-125a-3p, miR-214, miR-22, miR-320, miR-708, and miR-93), which in turn enhance NPCs proliferation and survivability. [score:12]
Protein kinase B or Akt, a key protein involved in the activation of PI3K-Akt pathway and is crucial in promoting cell survivability [43], is inhibited by the key microRNAs (miR-22, miR-214, miR-125a-3p, miR-320 and let-7 family) that are down-regulated with the addition of IGF-1. Chen et al. reported that down-regulation of miR-133b significantly overexpressed Akt1 mRNA, which increased T24 bladder cancer cell proliferation and reduced cell apoptosis [44]. [score:11]
However, BMSC-derived NPCs with addition of IGF-1 showed 12 microRNAs which include miR-22, miR-1224, miR-125a-3p, miR-214, miR-320, miR-708 and miR-93 were consistently down-regulated and only miR-496 remained up-regulated compared to Group C from Day 1 to Day 5. The let-7 family (let-7b, let-7c, let-7d, let-7e and let-7i) were constantly down-regulated in both groups. [score:9]
Furthermore, the introduction of IGF-1 triggers the down-regulation of several microRNAs (miR-214, miR-22, miR-320 and miR-708) with their inconsistent differential expression in Group A. The inhibition of miR-214 has been reported to decrease the level of apoptosis in HeLa cells [34]. [score:8]
The genes up-regulated by down-regulation of miR-22 (A); miR-125a-3p (B); let-7 family (C); miR-214 (D); and miR-320 (E) were analyzed using GeneMANIA web tool with default weighting method (i. e., weighting based to maximize connectivity between input genes). [score:7]
MicroRNAs Query Genes miR-22 Myc; Ets1; Tp53; Agt; Esr1; Pten; Akt1 miR-214 Bcl2; Adora1; Myc; Neurod1; Dhcr24; Kras; Fgfr1; Apc; pcgfr1; Prnp; Akt1 miR-125a-3p Bcl2; Egfr; Tp53; Apc; Akt1; Rela miR-320 Bcl2; Adora1; Acvr1; Neurod1; Dhcr24; Tp53; Hmox1; Nol3; Pten; Akt1; Cebpb Let-7 Family Cdkn1a; Tnf; Bcl2; Adora1; Egfr; Myc; Il10; Acvr1; Sycp3; Neurod1; Dhcr24; Cdkn1b; SMAD3; Kras; ras3; Neurod1Birc2; Tp53; Kcnh8; FN1; Fgfr1; Clu; Fas; Pten; Akt1; Rela; Cebpb We assessed the predicted target genes of the down-regulated microRNAs with the KEGG database. [score:6]
Query genes for individual microRNA are listed in Table 5. The major targeted genes by all or four out of five key microRNAs (miR-22, miR-214, miR-125a-3p, miR-320 and let-7 family) included Akt1, Tp53, Pten and Bcl2. [score:3]
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[+] score: 64
Rno-miR-19a, rno-miR-19b-2 and rno-miR-214 were downregulated at all four time-points, while rno-miR-137 was downregulated at T1 followed by upregulation from T2 to T4 (Fig.   6). [score:10]
Furthermore, we observed downregulated expression of miR-19a and miR-214, which are predicted to target ARC. [score:8]
The results of the present study indicate that propofol may have the ability to regulate the expression of rno-miR-19a, rno-miR-137, rno-miR-19b-2 and rno-miR-214 and their target genes, ARC and EGR2. [score:6]
The expression of four miRNAs (rno-miR-19a, rno-miR-137, rno-miR-19b-2 and rno-miR-214) and their target genes (EGR2 and ARC) were shown to be regulated by propofol in primary cultured embryonic NSCs. [score:6]
Rno-miR-19a (Rno, Rattus Norvegicus) and rno-miR-137, and their target gene EGR2, as well as rno-miR-19b-2 and rno-miR-214 and their target gene ARC were found to be closely related to neural developmental processes, including proliferation, differentiation, and maturation of NSCs. [score:6]
Recently, Huat et al. [49] found that the miR-214 was downregulated during the development of neural progenitor-like cell derived from rat bone marrow mesenchymal stem cell induced by IGF-1, bFGF and EGF. [score:5]
It can be speculated that the increased expression of ARC in NSCs following exposure to propofol will have a beneficial effect, which is in conflict with the neurotoxic effects of propofol in vivo reported by Krzisch et al. [10] Furthermore, when combined the patterns of miR-19a and miR-214 expression, the situation is much more complex and the results are somewhat contradictory. [score:5]
Relative expression levels of rno-miR-19b-2, rno-miR-137, rno-miR-19a and rno-miR-214 at all four time-points (immediately (T1), Day 1 (T2), Day 3 (T3) and Day 7 (T4) after treatment with propofol or DMSO). [score:3]
MiR-214 is located in the miR-199a–214 cluster and targets PTEN to produce a protective effect in cardiac myocytes against H [2]O [2] -induced injury [47]. [score:3]
In this way, we confirmed two genes (EGR2 and ARC) and four miRNAs (rno-miR-19a, rno-miR-137, rno-miR-19b-2 and rno-miR-214) that exhibited at least a 2-fold change in the mean expression level following propofol treatment at all four time-points. [score:3]
Fig. 6Quantitative RT-PCR analysis of relative expression levels of rno-miR-19b-2, rno-miR-137, rno-miR-19a and rno-miR-214. [score:3]
The fold-change in the mean expression levels of rno-miR-19b-2, rno-miR-137, rno-miR-19a and rno-miR-214 ranged from -2.56 to -12.15, -2.02 to 4.61, -2.33 to -6.68 and -2.16 to -4.63, respectively (Table  5). [score:3]
Lee et al. reported that miR-214 may act as a novel intermediator in controlling the NSC development [48]. [score:2]
The miRNAs predicted by all four databases (rno-miR-19b-2, rno-miR-137, rno-miR-19a and rno-miR-214, (Rno, Rattus Norvegicus)) were selected for validation (Table  4 and Fig.   5). [score:1]
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[+] score: 60
The microRNA-1, which targets sodium/calcium exchanger 1 (NCX), and microRNA-214, which targets sarcoplasmic reticulum calcium ATPase-2a (Serca2a), are involved in cardiac function regulation. [score:6]
Since the NCX gene was also validated as a target to miRNA-214, increased miRNA-214 has been suggested as a mechanism to downregulate the NCX in a pathological condition. [score:6]
Among the proteins related to Ca2+ handling, NCX is a validated target of miRNA-1, while Serca-2a is a predicted target of miRNA-214. [score:5]
In another study, Yang [19] found increased expression of miRNA-214 in cardiac tissue of patients with valvular diseases. [score:5]
MI induced a decrease in miRNA-1 expression and an increase in miRNA-214 expression. [score:5]
miR-214 is upregulated during ischemic injury and heart failure [19], but its role in these processes is unknown. [score:4]
In our study, the recovered expression of Serca-2a by miRNA-214 may represent one factor directly responsible for the improved cardiac function after ET. [score:4]
Yang T, Gu H, Chen X, Fu S, Wang C, Xu H, et al. Cardiac hypertrophy and dysfunction induced by overexpression of miR-214 in vivo. [score:3]
ET protocol after MI restored both miRNA-1 (23 %) and miRNA-214 expression to basal levels (Fig.   2a and b). [score:3]
On the other hand, in the T-INF group ET prevents the increase of the miRNA-214, which was associated with the expression of NCX in S-SHAM group, a known mechanism induced by ET to prevent Ca [2+] overload [1]. [score:3]
However, ET after MI partially restored miRNA-1 and returned miRNA-214 expression to basal levels. [score:3]
Through in silico analysis of predicted mRNA targets for miRNA, we found a conserved region on Serca-2a mRNA to miRNA-214 binding. [score:3]
Fig. 3Correlation between (a) miRNA-214 levels and Serca-2a protein expressionby western blot and (b) VO [2] max and miRNA-214 levels. [score:3]
However, we observed increased the NCX and it was not association with miRNA-214 in the S-INF group. [score:1]
However, the exact function of miRNA-214 in cardiac function has not yet been shown. [score:1]
Strong negative correlation was observed between Serca-2a and miRNA-214 (Fig.   3a) and between VO [2max] and miRNA-214 (Fig.   3b). [score:1]
Additionally, they observed in vivo that silencing miRNA-214 prevented cardiac hypertrophy and LV dysfunction in a pressure-overload mouse mo del of heart failure. [score:1]
The most interesting association observed in our study was with miRNA-214 and Serca-2a. [score:1]
Pearson correlation showed a strong correlation between Serca-2a and miRNA-214 in both the SHAM and INF groups. [score:1]
It can be observed in Fig.   2a and b that miRNA-1 decreased 52 % and miRNA-214 increased 54 % after MI. [score:1]
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[+] score: 47
microRNA-214 (miR-214) may target the phosphatase and tensin homolog deleted on chromosome ten (PTEN)based on bioinformatics analysis and some researches have reported that miR-214 could negatively regulate the PTEN expression by binding to its 3-UTR [14]. [score:6]
As shown in Fig. 7A, the expression of miR-214 at hippocampus had a significant difference among the three groups (p<0.05). [score:3]
miR-214 was predicted to be capable of targeting PTEN based on bioinformatics analysis and other related researches [14], [15]. [score:3]
In summary, in this study we have identified that chronic administration of high dose ketamine could induce the learning and memory impairment and increase the number of neuronal apoptotic cells of adolescent rats, in which the decreased miR-214 and increased PTEN expression might be involved. [score:3]
Among the different experimental treatments, the relative expression levels of miRNA-214 were calculated by using the following formula: relative gene expression  = 2 [−(ΔC] [T] [of experimental sample – ΔC] [T] [of control sample)]. [score:3]
In order to determine the corresponding ΔC [T] value, the C [T] value of the target gene miRNA-214 was subtracted from the U [6] C [T] value so as to normalize the values. [score:3]
The purpose of this study is to explore the potential effects of ketamine on learning and memory function, neuronal apoptosis and the expression of miR-214 and PTEN in adolescent rats. [score:3]
Rat hippocampal miRNA-214 expression was determined using quantitative reverse transcriptase-polymerase chain reaction (qRT-PCR) based upon the mirVana qRT-PCR miRNA kit manufacturer's instructions (Ambion Life technologies, USA). [score:3]
We therefore tested the effect of ketamine on the expression of miR-214 in the hippocampus of adolescent rats. [score:3]
In current study, we aimed to determine the effects of ketamine on learning and memory function, and neuronal apoptosis of adolescent rats and to assess the potential effects of ketamine on the expression of miR-214 and PTEN in hippocampus. [score:3]
The results showed that miR-214 expression level in high-dose ketamine group was lower than that in control or low-dose group. [score:3]
0099855.g007 Figure 7A: Quantitative analysis of hippocampus miR-214 levels in Control, K [1] and K [2] group, miR-214 expression were obviously decreased in K [2] group rats (n = 6; *p<0.05 compared with Control group or K [1] group). [score:2]
A: Quantitative analysis of hippocampus miR-214 levels in Control, K [1] and K [2] group, miR-214 expression were obviously decreased in K [2] group rats (n = 6; *p<0.05 compared with Control group or K [1] group). [score:2]
Relative miR-214 and PTEN protein expression levels in rat hippocampus were measured by qRT-PCR and western blot analysis. [score:1]
Hippocampal RNA extraction and qRT-PCR analysis of miRNA-214. [score:1]
10 rats in the sub group 3 were decapitated under deep anesthesia, then expression levels of the miR-214 and PTEN protein in the hippocampus were measured by qRT-PCR and western blot analysis respectively (n = 6). [score:1]
Further statistical analysis showed that relative miR-214 level in group K [2] was lower than that in Control or K [1] group [F [(2, 15)] = 250.734, p<0.01]. [score:1]
The miRNA-214 amplification and detection were performed using the Bio-Rad iCycler iQ 5 fluorescence PCR system (Bio-Rad, USA). [score:1]
The relative gene expression of miRNA-214 was calculated based on the number of PCR cycles of miRNA-214. [score:1]
qRT-PCR of miR-214 and western blot of PTEN protein. [score:1]
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[+] score: 43
Notably, rno-miR-214 was predicted to have maximum number of binding sites within the representative members of down-regulated pathways, whereas, rno-miR-34a was detected as miRNA hub having maximum number of interactions within the members of up-regulated pathways. [score:7]
Notably, miR-214 was predicted to anneal with the maximum number of significant genes (1,118 i. e. 583 down- and 535 up-regulated) and its seeds were more specific to down-regulated genes (Table 3 ). [score:7]
A few potential interactions are: rno-miR-214, -31, -199a-5p, -21, -34a and -132 were predicted to target several down-regulated TFs such as Hnf1α, Nfatc4 and Glis2. [score:6]
Similarly, 5 miRNAs (e. g., miR-214, -31 and -34a) were predicted to target down-regulated genes such as Glis2 and Hnf1α. [score:6]
Furthermore, Apc (down-regulated) was predicted as a putative target of miR-214 with a seed of 10nt long. [score:6]
These findings support our previous assumption in which we found that rno-miR-214 binding sites are abundantly present within down-regulated genes. [score:4]
Also, miR-214 and -503 were predicted to hybridise with Peroxisome proliferator-activated receptor α (Pparα) (down-regulated) with octamer seeds. [score:4]
Few examples include; rno-miR-214 can target Itgb4 (focal adhesion, ECM-receptor and actin cytoskeleton), Ccl19 (chemokine signaling), Mcm4 (cell cycle and DNA replication) and Tbl1x (Wnt signaling). [score:3]
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[+] score: 30
0125153.g009 Fig 9(A) Log2 plots of microarray and qPCR expression profiles for miRNAs and their predicted target genes: miR-214, and Xbp1; miR-29c, miR-200c and Klf4; and miR-30a, miR-200a, and Sox11. [score:5]
Xbp1 mRNA increased expression 6.5-fold across differentiation, while its targeting miR-214 decreased more than 10-fold (Fig 9A). [score:5]
Parotid acinar expression of Xbp1 is apparently maintained low in the embryo by dual repression entailing both direct repression by miR-214, and indirectly by Sox11 activating the Pax5 repressor. [score:5]
The observed decrease of miR-214 which may target Xbp1 mRNA, combined with the positive feedback loop between Xbp1 and Atf6 alpha [51, 52], would help maintain the observed elevated expression of Xbp1. [score:5]
S7 Fig(A) The human miR-214 binding site in the Xbp1 3'UTR is not conserved in rat (targetscan. [score:3]
The network suggests a molecular switch (involving Prdm1, Sox11, Pax5, miR-200a, and miR-30a) progressively decreases repression of Xbp1 gene transcription, in concert with decreased translational repression by miR-214. [score:3]
MiR-214 Target Sites in Rat Xbp1. [score:2]
Xbp1 3'UTR contains a known miR-214 binding site in humans [59]. [score:1]
Although this sequence is not conserved in rats (S7 Fig), the rat 3'UTR contains an alternate miR-214 predicted binding site, which was cloned into a reporter, and co-transfection experiments demonstrate repression of rat Xbp1 by miR-214 (Fig 9B). [score:1]
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[+] score: 29
Thus, since SERCA2a is an interesting target involved on cardiomyocyte function and is modulated by miRNA-214, we sought to determine the effects of RT on miRNA-214 expression and its target protein SERCA2a, and on the morphological and mechanical properties of isolated LV myocytes. [score:7]
On the other hand, Aurora et al. (2012) [47], reported that miRNA-214 targets both sodium/calcium exchanger 1 (NCX) and proapoptotic effectors of Ca [2+]-signaling pathways like CaMKII and cyclophilin D. Through in silico analysis of predicted targets for miRNA, we verified a possible relationship between SERCA2a and miRNA-214. [score:5]
Also, exercised animals exhibited faster cell contraction and relaxation, which can be explained by the decreased miRNA-214 expression and increased SERCA2a protein levels. [score:3]
SERCA2a expression levels were 18.5% higher in the TR group than in CO group (Figure 3B), which may be explained by the 18.5% decrease in the miRNA-214 level (Figure 3A). [score:3]
In addition, we have observed that trained animals exhibited faster cardiomyocyte contraction and relaxation, and that this adaptation is at least partly explained by improved SERCA2a expression and decrease of miRNA-214 with RT. [score:3]
The relative expression of miRNA-214 and U6 were analyzed by polymerase chain reaction (PCR), described as follows. [score:3]
Here, our results showed that decreased miRNA-214 levels in the trained group may explain the increased expression of SERCA2a. [score:3]
This relationship becomes of great interest because our results show that the regulation of SERCA2a by miRNA-214 occurs by exercise training. [score:2]
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Amongst these, miR-383 was differentially expressed in all three rats and up-regulated to the largest degree in rat one, and the ten other miRNAs, let-7d*, miR-181b, miR-187, miR-195, miR-214, miR-382, miR-411, miR-466b, miR-592 and miR-1224 were differentially expressed in at least two rats. [score:8]
In these 10 deregulated miRNAs, seven (let-7d*, miR-181b, miR-187, miR-214, miR-466b, miR-592, miR-1224) are up-regulated in two rats, and one (miR-195) is down-regulated. [score:8]
In dysregulated miRNAs, let-7d*, miR-181b, miR-187, miR-214, miR-383, miR-466b, miR-592, miR-1224 are significantly overexpressed in MrD compared to hippocampus, and miR-195 is downexpressed. [score:5]
Hence, miR-383 was differentially expressed in three rats, and let-7d*, miR-181b, miR-187, miR-195, miR-214, miR-382, miR-411, miR-466b, miR-592, miR-1224 were differentially expressed in two rats at least (Additional file 2: Table S4). [score:5]
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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]
Male-biased miRNA expression was associated with pathways related to cancer (miR-130b, miR-214, miR-181b, miR-199a, miR-150, miR-135a, miR-142-3p, miR-142-5p, miR-185), hematological disease (miR-22*, miR-142-3p, miR-142-5p, miR-150, miR-181b), and renal inflammation/nephritis (miR-130b, miR-223, miR-150, miR-142-5p, miR-296*, miR-185-3p) (Additional file 2). [score:5]
However, miR-214 exhibited sex-biased increase in expression at 104 weeks, showing 1.5 fold higher expression in males than in females. [score:5]
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]
For example, nine miRNAs (miR-21, miR-20a, miR-146a, miR-199a-3p, miR-214, miR-192, miR-187, miR-805, and miR-194) have been identified in C57BL/6 mice as promising biomarkers of kidney injury after renal ischemia reperfusion injury (IRI) [15]. [score:1]
These miRNAs showed high representation in renal inflammation and nephritis pathways, and included miR-214, miR-130b, miR-150, miR-223, miR-142-5p, miR-185, and miR-296*. [score:1]
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On the contrary, other microRNAs identified by these authors, such as miR-152, miR-214, miR-206, and miR-221, either did not show significant expression changes or showed opposite behaviors in our analyses (such as the downregulation of miR-1). [score:6]
Disagreements extend to other cell death-related microRNAs that were reported by Liu [6] to demonstrate changes in expression that we were not able to detect (mir-137 and miR-672) or whose expression did not seem to change in the present study (miR-214, miR-30-3p, miR-235-3p, and miR-674-5p). [score:5]
Expression changes respect to control/sham 1 dpo 7 dpo Name Liu Present Liu Present rno-miR-130b 1.42 NE rno-miR-146a 1.72 INC S rno-miR-15b 1.15 DEC NS rno-miR-17 1.74 INC NS rno-miR-18a 2.71 NE 3.41 NE rno-miR-200c 4.12 NE rno-miR-206 3.26 NE rno-miR-20a 1.69 NC rno-miR-20b-5p 1.83 NE rno-miR-21 1.37 INC S rno-miR-214 2.01 INC NS rno-miR-219-5p −1.82 DEC S rno-miR-221 1.1 NE rno-miR-223 3.58 INC S 3.4 INC S rno-miR-24-2* 2.41 DEC NS rno-miR-290 3.66 INC NS 2.96 DEC S rno-miR-378 1.31 INC NS rno-miR-410 −1.21 NE rno-miR-466b 3.05 DEC S rno-miR-541 1.11 INC S rno-miR-874 2,8 NEData restricted to microRNAs with significant changes in expression (2-fold or greater) according to Liu et al. [6]. [score:5]
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[+] score: 15
It has been reported that in human umbilical vein endothelial cells, Rg1 can downregulate miR-214 (a microRNA related closely to eNOS) expression, leading to an increase in eNOS expression [32]. [score:8]
Whether miR-214 downregulation is involved in the up-regulation of eNOS in this mo del used in our work remains to be studied. [score:7]
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[+] score: 13
In colon tissues from UC and ulcerative colitis -associated colorectal cancer (CRC) subjects, miR-214 expression was significantly upregulated to activate inflammatory responses; colon injury could be further aggravated through the feedback loop mediated by PTEN and PDLIM2, and the transcription factors NF- κB and STAT3 could be regulated to influence the IL-6 expression level. [score:9]
In contrast, miR-214 inhibitors reduced colitis in UC patients and tissues with DSS -induced colitis [40]. [score:3]
Five of these miRNAs were altered in colon tissues or peripheral blood in previous studies (miR-126, miR-214, miR-532, miR-140, and miR-340). [score:1]
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[+] score: 13
Of the 30 miRNAs they found upregulated in traumatic spinal cord injury, miR-223, miR-214, miR-20b-5p, miR-17, miR-146a, miR-199a-3p, miR-221-3p, miR-146b, and miR-145 were also upregulated in our study, and among the 16 downregulated miRNAs in traumatic spinal cord injury, miR-34a and miR-338 were also downregulated after ventral combined with dorsal root avulsion in our study. [score:13]
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[+] score: 11
In the mo del group, 17 miRNAs were downregulated, including miR-1, miR-133, miR-29, miR-126, miR-212, miR-499, miR-322, miR-378, and miR-30 family members, whereas the other 18 miRNAs were upregulated, including miR-21, miR-195, miR-155, miR-320, miR-125, miR-199, miR-214, miR-324, and miR-140 family members. [score:7]
Among these differentially expressed miRNAs, miR-1, miR-133, miR-29, miR-126, miR-499, miR-30, miR-21, miR-195, miR-155, miR-199, miR-214, and miR-140 have been reported to be related to MI [25– 36], while the other miRNAs have not been reported directly in MI. [score:4]
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[+] score: 11
12 of these miRNAs were ≥50% up-regulated in both groups with particularly strong increases in expression for miR-199a, miR-21, miR-214, miR-221, miR-222, and miR-31 (Figure 2B). [score:6]
Several miRNAs, including miR-21, miR-27, miR-31, miR-199a, miR-214 and miR-222 were up-regulated in these mouse mo dels in the same directions and to similar extents as observed in this study [11], [18]. [score:5]
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[+] score: 9
Among the miRNAs differentially expressed in Liu's study, rno-miR-132-3p, rno-miR-146b-5p, rno-miR-223-3p, rno-miR-21-5p, and rno-miR-214-3p were upregulated, which was just the same as our findings. [score:6]
In addition, as predicted by the bioinformatics databases, SLC4A1 was the potential target gene of rno-miR-34b, rno-miR-146b, rno-miR-214, rno-miR-223, and rno-miR-351. [score:3]
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[+] score: 9
The unique miRNA expression patterns distinguishing the ASH group from the control group were composed of six downregulated (miR-199a-3p, miR-214, miR-93, miR-146a, miR-191 and let-7b) and six upregulated (miR-129, miR-490, miR-21, miR-503, miR-183 and miR-185) miRNAs. [score:9]
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25
[+] score: 9
Also, microRNA-214 regulates expression of phosphatase and tensin homolog by activating PI3K/Akt pathway and downregulating caspase-3 expression to alleviate I/R -induced cardiomyocyte apoptosis [39]. [score:9]
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26
[+] score: 8
Among the miRNAs, miR-214, miR-199a-5p, miR-150, miR-199a-3p, miR-351, miR-145, miR-764, miR-497 and miR-92b were upregulated, whilst miR-7a, miR-325-5p, miR-485, miR-708, miR-344-3p, let-7f, miR-26b, miR-129, miR-29c and let-7a were downregulated. [score:7]
These miRNAs include miR-214, miR-199a-5p, miR-150, miR-351, miR-145, miR-92b, miR-7a, miR-485, miR-708, let-7f, miR-26b, miR-129, miR-29c and let-7a. [score:1]
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[+] score: 8
Balkom et al., (2013) showed that endothelial cells secrete exosomes containing miR-214, which suppress senescence and stimulates an angiogenetic program in target cell [17]. [score:5]
However, exosomal miR-214 expression in our study was not affected by age and CR (data not shown). [score:3]
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[+] score: 8
A putative explanation may derive from results on miR-214 expression in cancer, where downregulation of this microRNA inversely correlates with Pdrg1 expression [59], and accumulation of Polycomb Ezh2 methyltransferase is detected [74]. [score:8]
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[+] score: 8
Nine miRNAs (miR-21, miR-24, miR-214, miR-132, miR-195, miR-210, miR-144, miR-150 and miR-34a) were found in exosomes obtained from rats subjected to RIPC, but only miR-24 was significantly upregulated ([#] P < 0.05, n = 4). [score:4]
b, c Flow cytometric analysis of the uptake of exosomes by H9c2 cells at various time points We further determined the expression of nine miRNAs (miR-24, miR-21, miR-214, miR-132, miR-195, miR-210, miR-144, miR-150 and miR-34a) in both RIPC-EXO and EXO (Fig.   3a). [score:3]
Since the subject of our study was IRI, we selected nine miRNAs that have been reported to be involved either in oxidative stress (such as miR-150 and miR-21) 14, 15 or in cardiomyocyte apoptosis (such as miR-195, miR-132, miR-140, miR-144, miR-24, miR-214 and miR-34a) 16– 21 in our investigation and, using quantitative PCR (qPCR), explored whether RIPC could modify the expression level of these nine miRNAs in plasma exosomes. [score:1]
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[+] score: 7
miRNAs such as miR-1 [40, 41] and miR-214 [42], display anti-hypertrophic or cardioprotective effects by directly targeting 3′-UTR of Ncx1. [score:4]
Ncx1 has been validated as a target of miR-1 [40] and miR-214 [42]. [score:3]
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[+] score: 6
A recent study showed that inhibition of miR-495 increased neovascularization and recovery of blood flow after cardiac ischemia in mice [60], while miR-214 protected the mouse heart from ischemic injury by controlling Ca [2+] overload and cell death [61] (Table  5). [score:3]
For example, the top three miRNA-hubs in the early IR-injury regulatory network were rno-miR-495, rno-miR-214 and rno-miR-298, whereas rno-miR-873, rno-miR-223 and rno-miR-185 were hubs observed at the late phase post-IR injury. [score:2]
The top three rno-miRs at 24 h were rno-miR-495* (degree of 172), followed by rno-miR-214 (degree of 170) and rno-miR-207(degree of 143). [score:1]
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[+] score: 6
Other miRNAs from this paper: hsa-mir-16-1, hsa-mir-17, hsa-mir-20a, hsa-mir-21, hsa-mir-23a, hsa-mir-100, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-107, hsa-mir-16-2, mmu-mir-1a-1, mmu-mir-23b, mmu-mir-125b-2, mmu-mir-130a, mmu-mir-9-2, mmu-mir-145a, mmu-mir-181a-2, mmu-mir-184, mmu-mir-199a-1, hsa-mir-199a-1, mmu-mir-205, mmu-mir-206, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-199a-2, hsa-mir-205, hsa-mir-181a-1, hsa-mir-214, hsa-mir-219a-1, hsa-mir-223, mmu-mir-302a, hsa-mir-1-2, hsa-mir-23b, hsa-mir-125b-1, hsa-mir-130a, hsa-mir-145, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125b-2, hsa-mir-184, hsa-mir-206, mmu-mir-16-1, mmu-mir-16-2, mmu-mir-20a, mmu-mir-21a, mmu-mir-23a, mmu-mir-103-1, mmu-mir-103-2, rno-mir-338, mmu-mir-338, rno-mir-20a, hsa-mir-1-1, mmu-mir-1a-2, hsa-mir-181b-2, mmu-mir-107, mmu-mir-17, mmu-mir-100, mmu-mir-181a-1, mmu-mir-214, mmu-mir-219a-1, mmu-mir-223, mmu-mir-199a-2, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-181b-1, mmu-mir-125b-1, hsa-mir-302a, hsa-mir-219a-2, mmu-mir-219a-2, hsa-mir-302b, hsa-mir-302c, hsa-mir-302d, hsa-mir-367, hsa-mir-372, hsa-mir-338, mmu-mir-181b-2, rno-mir-9a-1, rno-mir-9a-3, rno-mir-9a-2, rno-mir-16, rno-mir-17-1, rno-mir-21, rno-mir-23a, rno-mir-23b, rno-mir-100, rno-mir-103-2, rno-mir-103-1, rno-mir-107, rno-mir-125b-1, rno-mir-125b-2, rno-mir-130a, rno-mir-145, rno-mir-181a-2, rno-mir-181b-1, rno-mir-181b-2, rno-mir-184, rno-mir-199a, rno-mir-205, rno-mir-206, rno-mir-181a-1, 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
In a similar fashion, another highly differentially expressed miRNA (miR-214) which displays a highly complementary alignment within the 3′ UTR of MOBP mRNA demonstrates a decrease in OP cells then a sharp increase in OLs. [score:3]
MiR-214 also shows a ∼34-fold decrease from the OP1 to OP2 transition and has a strong evolutionarily conserved 8mer target site to Mobp, which is important for providing the proper structural properties of myelin. [score:2]
The key miRNAs discussed in this manuscript were validated by conducting real-time qRT-PCR for samples from the appropriate stages, including the following: miR-199a and miR-145 at the OP1, OP2, OP3, and OL stages; miR-214 at the OP1 and OP2 stages; miR-184 and miR-1183 at the GP and OP1 stages (Table 1 ). [score:1]
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[+] score: 6
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]
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[+] score: 5
This mo del has proven to be useful in identifying key stress -induced microRNAs, such as miR-21 and miR-214 (Denby et al., 2011), which are upregulated during renal injury. [score:4]
miR-21 and miR-214 are consistently modulated during renal injury in rodent mo dels. [score:1]
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35
[+] score: 5
miR-214 targets ATF4 to inhibit bone formation. [score:5]
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36
[+] score: 4
Other miRNAs from this paper: rno-mir-103-2, rno-mir-103-1, rno-mir-132, rno-mir-139, rno-mir-487b
Wang showed that osteoblast-specific down-regulation of miR-214 levels could promote bone formation in HU mice, one of the three mo dels they used to research human aged osteoporosis 43. [score:4]
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Yang H. Kong W. He L. Zhao J. J. O'Donnell J. D. Wang J. Wenham R. M. Coppola D. Kruk P. A. Nicosia S. V. Microrna expression profiling in human ovarian cancer: Mir-214 induces cell survival and cisplatin resistance by targeting pten Cancer Res. [score:4]
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Figure  2 shows that whilst the expression of miR26a, miR200b, miR214, miR218, and let-7d was not altered in arteries from SHRs compared with NT, a significant increase of miR153 was recorded in SHR MA (8.65, N = 6, P < 0.0001), RA (2.08, N = 6, P < 0.0001), and TA (2.80, N = 6, P < 0.0001). [score:2]
This analysis revealed putative seed sequences in KCNQ4 for miR26a, miR214, miR133a, miR200b, miR153, miR218, and let-7d. [score:1]
In silico analysis of the 3′ UTR of KCNQ4 revealed seed sequences for miR26a, miR133a, miR200b, miR153, miR214, miR218, and let-7d with quantitative polymerase chain reaction showing miR153 increased in those arteries from SHRs that exhibited decreased Kv7.4 levels. [score:1]
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[+] score: 4
Yuan Y MicroRNA-98 and microRNA-214 post-transcriptionally regulate enhancer of zeste homolog 2 and inhibit migration and invasion in human esophageal squamous cell carcinomaMol Cancer. [score:4]
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40
[+] score: 4
Studies to examine the dose- and time- dependent regulation of miR-214 and miR-125a, by androgens, are ongoing in our laboratories. [score:2]
However, only two miRs, miR-214 and miR-125a, positively correlated with androgen action in prostate. [score:1]
Detection of miRs in serum miR-214 and miR-125a. [score:1]
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41
[+] score: 4
Other miRNAs from this paper: rno-mir-21, rno-mir-132, rno-mir-145, rno-mir-222, rno-mir-223
Several miRNAs, including miR-222 as well as miR-21 and miR-214, have been established as regulators of PTEN expression [41], [42]. [score:4]
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42
[+] score: 4
Recently, Li et al. reported that 16 miRNAs including miR-34, miR-199a-5p, miR-221, miR-146b, and miR-214 showed progressive up-regulation in rat with hepatic fibrosis caused by dimethylnitrosamine [30]. [score:4]
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43
[+] score: 4
Other miRNAs from this paper: hsa-mir-26a-1, hsa-mir-214, hsa-mir-26a-2, rno-mir-26a
In particular, microRNAs miR-26a and miR-214 repress EZH2 posttranscriptionally during skeletal muscle cell and ESC differentiation and establish a regulatory loop controlling EZH2 -dependent gene expression during differentiation (Juan et al, 2009; Wong & Tellam, 2008). [score:4]
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44
[+] score: 3
Sun et al. provided evidences and testified that osteoclasts secreted circulating miR-214 to inhibit osteoblast activity[18]. [score:3]
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45
[+] score: 3
At 24 hours, five miRNAs (rno-miR-214, rno-miR-99a, rno-miR-363*, rno-miR-100 and rno-miR-340–5p) and at 48 hrs 6 miRNAs (rno-miR-34b, rno-miR-500, rno-miR-24-1*, rno-miR-29b, rno-miR-199a-3p, rno-let-7a) showed the most prominent dysregulation (P < 0.001) (Fig.   7B). [score:2]
MicroRNA profiling identified several miRNAs that have been previously associated with cardiac hypertrophy such as miR-214, miR-23b, miR-15b, rno-miR-26b, rno-miR-221, rno-miR-222, rno-miR-107 [59], miR-23a, miR-208, rno-miR-133b, miR-19a and mi-r133a [60]. [score:1]
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[+] score: 3
Eleven miRNAs, including miR-145-5p, miR-34c-5p, miR-365-3p, miR-214-3p, miR-151, miR-27a, miR-153-5p, miR-365-3p, miR-33-5p, miR-217-5p and miR-129-5p, were differentially and significantly expressed (P < 0.05; Figure 2B). [score:3]
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47
[+] score: 3
Similarly, increased liver expression of miR-93, miR-214, and miR-669c has been correlated with age. [score:3]
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48
[+] score: 3
Li et al. pointed out that cir-ITCH interacted with 3 molecules of miR-7, miR-17 and miR-214 to increase the level of ITCH and suppress the ESCC [20]. [score:3]
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49
[+] score: 3
Two genes (miR-345-3p and miR-214) with most stable expression across samples (with highest P-value and lowest SD in Multi-Factor ANOVA analysis) were tested by qPCR in Ago2 IP (n = 6) and input samples (n = 6) in both treated and control dentate gyrus obtained at 30 min post-HFS. [score:3]
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[+] score: 3
Other miRNAs from this paper: rno-mir-21, rno-mir-22, rno-mir-217
However, to date, few miRNAs have been found to execute their biological functions in DN by targeting PTEN, such as miR-21, miR-214, and miR-217 [20– 22]. [score:3]
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51
[+] score: 2
For example, Pparα (regulates metabolic pathways) was found to harbor putative binding sites for miR-19b/351 (5 algorithms), miR-17-5p (3 algorithms), miR-214 and -503 (2 algorithms). [score:2]
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Name Primers U6F: 5′-GCTTCGGCAGCACATATACTAAAAT-3′ R: 5′-CGCTTCACGAATTTGCGTGTCAT-3′ rno-miR-500-3pGSP: 5′-GGAAGGCACCTGGGCAAG-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-499-3pGSP: 5′-GGGGAACATCACAGCAAGTC-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-214-3pGSP: 5′-GGGGACAGCAGGCACAGAC-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-20b-5pGSP: 5′-GGGGCAAAGTGCTCATAGTG-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-877GSP: 5′-GGGGAAGTAGAGGAGATGGC-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-451-5pGSP: 5′-GGGGGAAACCGTTACCATTAC-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-3577GSP: 5′-GGGTTCTGTCCCTCTTGGC-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-370-3pGSP: 5′-AGCCTGCTGGGGTGGAA-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-181d-5pGSP: 5′-GGGGCATTCATTGTTGTCG-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-23b-3pGSP: 5′-GGGATCACATTGCCAGGG-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-191a-5pGSP: 5′-GGCAACGGAATCCCAAAAG-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-200c-3pGSP: 5′-GGGGTAATACTGCCGGGTAA-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-328a-3pGSP: 5′-AACTCGCCCTCTCTGCCC-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ nutrients-07-01333-t002_Table 2 Table 2 Primers of mRNA targets. [score:1]
Name Primers U6F: 5′-GCTTCGGCAGCACATATACTAAAAT-3′ R: 5′-CGCTTCACGAATTTGCGTGTCAT-3′ rno-miR-500-3pGSP: 5′-GGAAGGCACCTGGGCAAG-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-499-3pGSP: 5′-GGGGAACATCACAGCAAGTC-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-214-3pGSP: 5′-GGGGACAGCAGGCACAGAC-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-20b-5pGSP: 5′-GGGGCAAAGTGCTCATAGTG-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-877GSP: 5′-GGGGAAGTAGAGGAGATGGC-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-451-5pGSP: 5′-GGGGGAAACCGTTACCATTAC-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-3577GSP: 5′-GGGTTCTGTCCCTCTTGGC-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-370-3pGSP: 5′-AGCCTGCTGGGGTGGAA-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-181d-5pGSP: 5′-GGGGCATTCATTGTTGTCG-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-23b-3pGSP: 5′-GGGATCACATTGCCAGGG-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-191a-5pGSP: 5′-GGCAACGGAATCCCAAAAG-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-200c-3pGSP: 5′-GGGGTAATACTGCCGGGTAA-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ rno-miR-328a-3pGSP: 5′-AACTCGCCCTCTCTGCCC-3′ R: 5′-GTGCGTGTCGTGGAGTCG-3′ nutrients-07-01333-t002_Table 2 Table 2 Primers of mRNA targets. [score:1]
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53
[+] score: 2
EA pretreatment had a protective effect on ischemia/reperfusion injury via miR-214 (Liu et al., 2014) and miR-124 (Chen S. H. et al., 2016). [score:1]
Mediated protective effect of electroacupuncture pretreatment by miR-214 on myocardial ischemia/reperfusion injury. [score:1]
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54
[+] score: 2
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]
5 mmu-miR-214 -1.7 -6.1 -10.9 mmu-miR-137 -31.7 -6.8 -144.8 mmu-miR-29c -1.8 -10.5 -10.7 rno-miR-532–5p -2.0 -59.1 -126.9 mmu-miR-466d-3p -2.7 -4.2 -9.9 mmu-miR-466d-5p -23.2 -64.7 -105.7 mmu-miR-22 -1.6 -4.6 -9.9 mmu-miR-582–5p -21.3 -59.4 -97.1 mmu-miR-690 -1.9 -2.1 -9.7 rno-miR-421 -21.3 -59.3 -97.0 mmu-miR-193 -4.9 -3. 5 -8.1 mmu-miR-369–5p -20.9 -58.3 -95.3 mmu-miR-27b* -2.1 -2.9 -8.0 mmu-miR-684 -20.8 -58.1 -94.9 mmu-miR-378 -1.6 -4.6 -7.7 mmu-miR-375 -20.6 -57.6 -94.2 mmu-miR-9* -1.9 -18.4 -7.7 mmu-miR-337–5p -20.5 -57.4 -93.8 mmu-miR-204 -2.5 -5.3 -7.5 mmu-miR-15a* -20.3 -56.8 -92.8 mmu-miR-28* -1.9 -3.2 -6.5 mmu-miR-532–5p -19. [score:1]
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55
[+] score: 2
Other miRNAs from this paper: hsa-mir-214
Resistance training regulates cardiac function through modulation of miRNA-214. [score:2]
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56
[+] score: 1
Mediated protective effect of electroacupuncture pretreatment by miR-214 on myocardial ischemia/reperfusion injury. [score:1]
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57
[+] score: 1
Other miRNAs from this paper: rno-mir-27a, rno-mir-196a, rno-mir-206
Chen L et al. 15 have demonstrated that miR-214 is delivered by EVs in hepatic fibrosis. [score:1]
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58
[+] score: 1
Furthermore, several miRNAs, such as miR-199a and miR-214 [14], miR-494 [15], miR-499 [16], and miR-24 [17] are known to protect cells from hypoxia- or ischemia -induced damage. [score:1]
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The following miRNAs were found to be altered in aging rats mostly from 48 weeks–132 weeks of age in skeletal muscle, e. g., miR-22 [57], or in murine liver tissues, e. g., miR-669c and miR-709, miR-93 and miR-214 [58, 59]. [score:1]
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