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63 publications mentioning rno-mir-126b

Open access articles that are associated with the species Rattus norvegicus and mention the gene name mir-126b. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 457
Other miRNAs from this paper: mmu-mir-126a, rno-mir-126a, mmu-mir-126b
Compared with the adjacent normal tissues, the miR-126 expression in HCC tissues was downregulated while EGFL7 and ERK mRNA expressions were upregulated (all P < 0.05), indicating low miR-126 expression and high EGFL7 and ERK expressions might promote the risk of HCC. [score:14]
In the miR-126 inhibitors group, the miR-126 expression and Fas/FasL and Caspase3 mRNA expressions were evidently downregulated while EGFL7, ERK, and Bcl-2 mRNA expressions were markedly upregulated when compared with the blank group (all P < 0.05). [score:14]
Three transfected cell lines (HepG2, Bet-7402 and smmc-7721) were separately divided into the blank group (without transfection), the miR-126 mimics group (transfected with miR-126 mimics plasmid), the miR-126 inhibitors group (transfected with miR-126 inhibitors plasmid), the miR-126 inhibitors + si-EGFL7 group (transfected with miR-126 inhibitors + si-EGFL7 plasmid), the mimics control group (transfected with miR-126 mimics NC plasmid), and the inhibitors control group (transfected with miR-126 inhibitors NC plasmid). [score:13]
Rats injected with the same cell line were assigned into six groups (8 mice in each group): the blank group (injection of cells without transfected plasmids); the miR-126 mimics group (injection of cells being transfected with miR-126 mimics plasmid); the miR-126 inhibitors group (injection of cells being transfected with miR-126 inhibitors plasmid); the miR-126 inhibitors + siRNA EGFL7 group (injection of cells being transfected with miR-126 inhibitors + siRNA EGFL7 plasmids); the mimics control group (injection of cells being transfected with miR-126 mimics NC plasmid); and the inhibitors control group (injection of cells being transfected with miR-126 inhibitors NC plasmid). [score:13]
Compared with the blank group,, Fas/FasL and Caspase3 protein expressions were decreased, and EGFL7, ERK, P-ERK, Bcl-2 protein expressions were significantly increased in the miR-126 inhibitors group (all P < 0.05), suggesting that the low EGFL7 expression inhibited the activation of the ERK signaling pathway, promoting the expression of pro-apoptotic factors and HCC cell apoptosis [20]. [score:12]
the proliferation of smmc-7721 cells among the blank, miR-126 mimics, miR-126 inhibitors, miR-126 inhibitors + siRNA EGFL7, mimics control and inhibitors control groups after transfection; * P < 0.05 compared with the blank group; miR-126, microRNA-126; EGFL7, epidermal growth factor-like domain 7. After three HCC cell lines (smmc-7721, Bet-7402, and HepG2) were transfected with the recombinant plasmids, the apoptosis rate of HCC cells was significantly increased in the miR-126 mimics group and that of HCC cells was reduced in the miR-126 inhibitors group compared with the blank group, indicating that miR-126 overexpression could induce the apoptosis of HCC cells (Figure 7). [score:9]
, Hercules, CA, USA) was applied to analyze miR-126 expression and expressions of EGFL7 and ERK mRNAs in HCC tissues and adjacent normal tissues as well as the miR-126 expression and expressions of EGFL7, ERK, Fas/FasL, Bcl-2, and Caspase-3 mRNAs in the transfected cells. [score:9]
Therefore, the miR-126 overexpression and inhibition of EGFL7 expression might suppress the proliferation ability of tumor cells in vivo. [score:9]
These results indicated that miR-126 overexpression and inhibition of EGFL7 expression could suppress the proliferation of HCC cells. [score:9]
Our initial results revealed that miR-126 is significantly downregulated, while the mRNA and protein expression of EGFL7 and ERK are upregulated in HCC tissues. [score:9]
miR-126 overexpression inhibited expressions of EGFL7, ERK, P-ERK, angiogenesis -associated proteins VEGF, and CD31 in HCC cells in vivoThe EGFL7 expression was the highest in smmc-7721 cells in vivo, and lowest in HepG2 cells among three HCC cells lines which was transfected with recombinant plasmids (Figure 9). [score:9]
Compared with the blank group, no significant difference was observed in the miR-126 expression and expressions of EGFL7, ERK, Fas/FasL, Bcl-2 and Caspase3 mRNAs in the miR-126 inhibitors + si-EGFL7, mimics control and inhibitors control groups (all P > 0.05). [score:8]
In the miR-126 mimics group, the miR-126 expression and Fas/FasL and Caspase3 mRNA expressions were significantly increased and the EGFL7, ERK, and Bcl-2 mRNA expressions were notably decreased in comparison to the blank group (all P > 0.05). [score:7]
Comparison of cell proliferation among the blank, miR-126 mimics, miR-126 inhibitors, miR-126 inhibitors + siRNA EGFL7, mimics control, and inhibitors control groups after transfection. [score:7]
miR-126 overexpression inhibited expressions of EGFL7, ERK, P-ERK, angiogenesis -associated proteins VEGF, and CD31 in HCC cells in vivo. [score:7]
the proliferation of HepG2 cells among the blank, miR-126 mimics, miR-126 inhibitors, miR-126 inhibitors + siRNA EGFL7, mimics control and inhibitors control groups after transfection; (B). [score:7]
No significant difference was observed in EGFL7, ERK, P-ERK, VEGF, and CD31 protein expressions among the blank, miR-126 inhibitors + si-EGFL7, mimics control and inhibitors control groups (all P > 0.05). [score:7]
the proliferation of Bet-7402 cells among the blank, miR-126 mimics, miR-126 inhibitors, miR-126 inhibitors + siRNA EGFL7, mimics control and inhibitors control groups after transfection; (C). [score:7]
Comparisons of cell apoptosis among the blank, miR-126 mimics, miR-126 inhibitors, miR-126 inhibitors + siRNA EGFL7, mimics control and inhibitors control groups in smmc-7721, Bet-7402, and HepG2 cell lines after transfection (× 400). [score:7]
Tumor growth curves of nude mice transplanted with smmc-7721, Bet-7402 and HepG2 cell lines in the blank, miR-126 mimics, miR-126 inhibitors, miR-126 inhibitors + siRNA EGFL7, mimics control and inhibitors control groups. [score:7]
MiR-126 expression is downregulated in human cancers, reducing its ability to suppress the proliferative and invasive capacities of cancer cells, such as lung cancer, osteosarcoma, oral cancer and so on [11, 12, 21]. [score:7]
These results showed that miR-126 overexpression could reduce the expression of ERK, P-ERK and angiogenesis -associated proteins, inhibiting tumor angiogenesis and tumor growth. [score:7]
Compared with the blank group, no significant difference was observed in the expressions of EGFL7, ERK, P-ERK, Bcl-2 Fas/FasL and Caspase3 proteins in the miR-126 inhibitors + si-EGFL7, mimics control, and inhibitors control groups (all P > 0.05). [score:6]
To conclude, our study shows that miR-126 is downregulated in HCC tissues and that elevated miR-126 decreases proliferation and induces apoptosis in the HCC cells and inhibits angiogenesis. [score:6]
the proliferation of smmc-7721 cells among the blank, miR-126 mimics, miR-126 inhibitors, miR-126 inhibitors + siRNA EGFL7, mimics control and inhibitors control groups after transfection; * P < 0.05 compared with the blank group; miR-126, microRNA-126; EGFL7, epidermal growth factor-like domain 7. (A). [score:6]
Moreover, overexpression of miR-126 inhibits angiogenesis triggered by the HCC cells. [score:5]
miR-126 serves as a tumor suppressor, inhibiting cell proliferation and inducing cell apoptosis in HCC [14]. [score:5]
No significant difference was observed in the proliferation of HCC cells in the miR-126 inhibitors + si-EGFL7, mimics control and inhibitors control groups in comparison to the blank group (all P > 0.05). [score:5]
A mechanism of miR-126 targeting EGFL7 to inhibit cell proliferation has also been confirmed by Sun et al. in non-small cell lung cancer [25]. [score:5]
Therefore, the miR-126 overexpression could inhibit tumor angiogenesis. [score:5]
miR-126 overexpression suppressed the proliferation of HCC cells. [score:5]
comparisons of miR-126 expression and EGFL7, ERK, Fas/FasL, Bcl-2, and Caspase-3 mRNA expressions in HepG2 cells among the six groups; (C). [score:5]
And then these three cell lines were separately transfected with recombinant plasmids (pLEGFP-N1-miR-126 mimic, pLEGFP-N1-miR-126 inhibitor, pLEGFP-N1-miR-126 mimic NC, pLEGFP-N1-miR-126 inhibitor NC or pLEGFP-N1-si EGFL7) using Lipofectamine 2000 and then incubated in an incubator containing 5% CO [2] at 37°C for 6 h. Next, cells were cultured with fresh medium containing 10% fetal bovine serum (FBS) for 48 h. Subsequently, cells were collected and washed with phosphate buffered saline (PBS) 3 times. [score:5]
EGFL7, ERK, P-ERK, VEGF, and CD31 protein expressions were decreased in the miR-126 mimics group, but these were significantly elevated in the miR-126 inhibitors group relative to the blank group (all P < 0.05). [score:5]
HepG2, Bet-7402, and smmc-7721 cells were transfected with recombinant plasmids (pLEGFP-N1-miR-126 mimic, pLEGFP-N1-miR-126 inhibitor, pLEGFP-N1-miR-126 mimic NC, pLEGFP-N1-miR-126 inhibitor NC, or pLEGFP-N1-si EGFL7). [score:5]
The transfection efficiency of recombinant plasmids pLEGFP-N1-miR-126 mimic, pLEGFP-N1-miR-126 inhibitor, pLEGFP-N1-miR-126 mimic NC, pLEGFP-N1-miR-126 inhibitor NC and pLEGFP-N1-si EGFL7 determined by flow cytometry. [score:5]
comparison of miR-126 expression and EGFL7, ERK, Fas/FasL, Bcl-2, and Caspase-3 mRNA expressions in Bet-7402 cells among the six groups; (D). [score:5]
miR-126 expression and EGFL7, ERK, Fas/FasL, Bcl-2, and Caspase-3 mRNA expression in HCC tissues, adjacent normal tissues, and transfected HCC cell lines. [score:5]
The miR-126 mimics group exhibited markedly higher Fas/FasL and Caspase3 protein expressions and lower EGFL7, ERK, P-ERK, and Bcl-2 protein expressions than the blank group (all P > 0.05). [score:5]
Human mature miR-126 mimics, miR-126 inhibitors, miR-126 mimics control, and miR-126 inhibitors control were purchased from Biomics Biotechnologies Co. [score:5]
Therefore, the corresponding recombinant plasmids including pLEGFP-N1-miR-126 mimic, pLEGFP-N1-miR-126 inhibitor, pLEGFP-N1-miR-126 mimic negative control (NC), pLEGFP-N1-miR-126 inhibitor NC, and pLEGFP-N1-si EGFL7. [score:5]
Zhao et al. have also demonstrated that the high miR-126 expression can inhibit cell proliferation, arrest cell cycle progress, and induce apoptosis in HCC cells [14], which is consistent with our study. [score:5]
No significant difference in the number of new blood vessels was observed among the blank, miR-126 inhibitors + si-EGFL7, mimics control, and inhibitors control groups (all P > 0.05). [score:5]
The proliferation of HCC cells might be enhanced when miR-126 expression was suppressed. [score:5]
comparisons of miR-126 expression and EGFL7 and ERK mRNA expression between the HCC tissues and adjacent normal tissues; (B). [score:5]
comparisons of miR-126 expression and EGFL7, ERK, Fas/FasL, Bcl-2 and Caspase-3 mRNA expressions in smmc-7721 cells among the six groups; [#] P < 0.05 compared with adjacent normal tissues; * P < 0.05 compared with the blank group; HCC, hepatocellular carcinoma; miR-126, microRNA-126; EGFL7, epidermal growth factor-like domain 7; ERK, extracellular signal-regulated kinase; FASL, FAS ligand; Bcl-2, B cell leukemia/lymphoma-2. (A). [score:4]
EGFL7: the direct target gene of miR-126. [score:4]
Moreover, miR-126 could reduce cell proliferation and tumor angiogenesis of HCC via decreasing EGFL7 expression [26], which is similar to our results, but the negative regulation of miR-126 on ERK signaling pathway was not involved. [score:4]
comparisons of miR-126 expression and EGFL7, ERK, Fas/FasL, Bcl-2 and Caspase-3 mRNA expressions in smmc-7721 cells among the six groups; [#] P < 0.05 compared with adjacent normal tissues; * P < 0.05 compared with the blank group; HCC, hepatocellular carcinoma; miR-126, microRNA-126; EGFL7, epidermal growth factor-like domain 7; ERK, extracellular signal-regulated kinase; FASL, FAS ligand; Bcl-2, B cell leukemia/lymphoma-2. Figure 3(A). [score:4]
The effects of miR-126 on HCC cells may be achieved by targeting EGFL7 and down -regulating the ERK signaling pathway. [score:4]
miR-126 is dysregulated in many human cancers, modulating the proliferation, migration, and invasion of cancer cells in conjunction with various target genes [11– 13]. [score:4]
The results indicated that EGFL7 was the direct target gene of miR-126. [score:4]
Further experiments indicated that the function of miR-126 in HCC is achieved by targeting EGFL7 and subsequently regulating of the ERK signaling pathway. [score:4]
The mice were sacrificed after three weeks, and no significant difference was observed in tumor volume and weight of the miR-126 inhibitors + si-EGFL7, mimics control and inhibitors control groups compared with the blank group (all P > 0.05). [score:4]
comparisons of miR-126 expression and EGFL7, ERK, Fas/FasL, Bcl-2 and Caspase-3 mRNA expressions in smmc-7721 cells among the six groups; [#] P < 0.05 compared with adjacent normal tissues; * P < 0.05 compared with the blank group; HCC, hepatocellular carcinoma; miR-126, microRNA-126; EGFL7, epidermal growth factor-like domain 7; ERK, extracellular signal-regulated kinase; FASL, FAS ligand; Bcl-2, B cell leukemia/lymphoma-2. Figure 3(A). [score:4]
Our study also demonstrates that overexpressed miR-126 decreases cell proliferation and induces cell apoptosis in HCC cells. [score:3]
Additionally, De Giorgio et al. have reported the loss of miR-126 may enhance angiogenesis through target specific proangiogenic factors at the in situ to invasive tumor transition, which could further prove our results [35]. [score:3]
The tumor weight in the miR-126 mimics group was decreased and the tumor weight in the miR-126 inhibitors group was evidently increased than that in the blank group (Table 3). [score:3]
Wong et al. have found that miR-126 is significantly decreased in patients carrying hepatitis B and C virus, and lower miR-126 expression predicts poor survival and tumor recurrence for HCC patients after surgery [22]. [score:3]
miR-126 overexpression induced tumor angiogenesis of HCC cells in vivoThe number of new blood vessels was the highest in the nude mice transplanted with smmc-7721 cells, and that was lowest in the nude mice transplanted with HepG2 cells among the three HCC cell lines which were transfected with recombinant plasmids (Table 3). [score:3]
However, the full understanding of miR-126 with ERK signaling in HCC is still uncertain, and more researches are still required to identify and effective targeted treatment for HCC. [score:3]
In this study, we showed that miR-126 was significantly reduced in HCC tissues, and the elevation of miR-126 could decrease cell proliferation, induce cell apoptosis, and inhibit angiogenesis in HCC cells. [score:3]
miR-126 expression was negatively correlated with EGFL7 and ERK levels in HCC tissues and cell lines. [score:3]
The levels of ERK and Bcl-2 mRNA and protein were elevated in the miR-126 inhibitors group, while those of Fas/FasL and Caspase-3 were reduced. [score:3]
miR-126 overexpression reduced the proliferation of HCC cells in vivoThe subcutaneous tumor volume in nude mice was gradually increased three days after transplantation. [score:3]
miR-126 overexpression promoted the apoptosis of HCC cells. [score:3]
These results showed that miR-126 expression was negatively correlated with EGFL7 and ERK (Figures 2, 3). [score:3]
The proliferation ability of tumor cells might be enhanced by the inhibition of miR-126. [score:3]
Additionally, our study has indicated that EGFL7 is the target gene of miR-126. [score:3]
EGFL7, ERK, P-ERK, VEGF and CD31 protein expression in smmc-7721 cells in vivo; * P < 0.05 compared with the blank group; miR-126, microRNA-126; EGFL7, epidermal growth factor-like domain 7; ERK, extracellular signal-regulated kinase; P-ERK, phosphorylated ERK; VEGF, vascular endothelial growth factor. [score:3]
EGFL7, ERK, VEGF, and CD31 protein levels are reduced in the miR-126 mimics group, while EGFL7, ERK, P-ERK, VEGF, and CD31 protein are increased in the miR-126 inhibitors group. [score:3]
Among three HCC cell lines (HepG2, Bet-7402 and smmc-7721), the lowest miR-126 expression was observed in smmc-7721 cells, and the highest in HepG2 cells. [score:3]
MiR-126 overexpression using miR-126 mimics could significantly reduce the phosphorylation of ERK protein [24]. [score:3]
Saito et al. reported that miR-126 is situated within the gene for epidermal growth factor-like domain 7 (EGFL7), which is highly expressed in vascularized tissues and endothelial cells and acts as an important gene in angiogenesis [15]. [score:3]
The miR-126 mimics group had markedly less new blood vessels and that in the miR-126 inhibitors group exhibited significantly more new blood vessels than the blank group (both P < 0.05). [score:3]
The miR-126 inhibitors group exhibited the strongest tumor formation ability with faster tumor cell growth and the miR-126 mimics group had the weakest tumor formation ability with slower tumor cell growth among the six groups (Figure 8). [score:3]
miR-126 overexpression induced tumor angiogenesis of HCC cells in vivo. [score:3]
miR-126 overexpression reduced the proliferation of HCC cells in vivo. [score:3]
The targeting gene (EGFL7) of miR-126 was predicted using microRNA. [score:3]
Identification of miR-126 targeting EGFL7. [score:3]
r, correlated coefficient; r > 0, positive correlation; r < 0, negative correlation; miR-126, microRNA-126; EGFL7, epidermal growth factor-like domain 7; ERK, extracellular signal-regulated kinase; HCC, hepatocellular carcinoma. [score:2]
the luciferase activity at 48 h after the HepG2 cells were transfected with EGFL7-3′UTR-WT + NC, EGFL7-3′UTR-WT + miR-126, EGFL7-3′UTR-MUT + NC and EGFL7-3′UTR-MUT + miR-126; * P < 0.05 compared with cells transfected with EGFL7-3′UTR-WT + NC, EGFL7-3′UTR-MUT + NC or EGFL7-3′UTR-MUT + miR-126; miR-126, microRNA-126; EGFL7, epidermal growth factor-like domain 7; NC, negative control; 3′UTR, 3′ untranslated region; WT, wide type; MUT, mutant type. [score:2]
The target gene of miR-126 was identified with dual-luciferase reporter assay. [score:2]
Compared with the blank group, the proliferation of HCC cells in the miR-126 mimics group was decreased while that of HCC cells in the miR-126 inhibitors group was increased significantly (both P < 0.05). [score:2]
comparisons of the expressions of EGFL7, ERK, P-ERK, Fas/FasL, Bcl-2 and Caspase-3 proteins in smmc-7721 cells among the six group; [#] P < 0.05 compared with adjacent normal tissues; * P < 0.05 compared with the blank group; HCC, hepatocellular carcinoma; miR-126, microRNA-126; EGFL7, epidermal growth factor-like domain 7; ERK, extracellular signal-regulated kinase. [score:2]
Note: DAPI dye cell nucleus was blue; miR-126, microRNA-126; EGFL7, epidermal growth factor-like domain 7; DAPI, 4′-6-diamidino-2-phenylindole. [score:1]
A. transfection efficiency of recombinant plasmids in HepG2 cells; B. transfection efficiency of recombinant plasmids in Bet-7402 cells; C. transfection efficiency of recombinant plasmids in smmc-7721 cells; miR-126, microRNA-126; EGFL7, epidermal growth factor-like domain 7; NC, negative control. [score:1]
Meanwhile, cells co -transfected with EGFL7-3′UTR-WT and NC plasmids (EGFL7-3′UTR-WT + NC) and with EGFL7-3′UTR-MUT and miR-126 mimic plasmids (EGFL7-3′UTR-MUT + miR-126) as controls. [score:1]
the binding site of miR-126 and EGFL7 in the 3′UTR; (B). [score:1]
Figure 7 Note: DAPI dye cell nucleus was blue; miR-126, microRNA-126; EGFL7, epidermal growth factor-like domain 7; DAPI, 4′-6-diamidino-2-phenylindole. [score:1]
correlation analysis of miR-126, EGFL7, and ERK in HCC tissues and adjacent normal tissues. [score:1]
Figure 1 A. transfection efficiency of recombinant plasmids in HepG2 cells; B. transfection efficiency of recombinant plasmids in Bet-7402 cells; C. transfection efficiency of recombinant plasmids in smmc-7721 cells; miR-126, microRNA-126; EGFL7, epidermal growth factor-like domain 7; NC, negative control. [score:1]
miR-126 had no effect on cell cycle distribution of HCC cells. [score:1]
org predicted that miR-126 was located in the introns 6 and 7 in the 3′-UTR of EGFL7 and could bind to the 3′-UTR of EGFL7 mRNA. [score:1]
We found that ERK and Bcl-2 mRNA and protein levels are significantly reduced in the miR-126 mimics group, while those of Fas/FasL and Caspase-3 are increased. [score:1]
correlation analysis of miR-126 and ERK in adjacent normal tissues; (B), correlation analysis of miR-126 and EGFL7 in adjacent normal tissues; (C), correlation analysis of miR-126 and ERK in HCC tissues; (D), correlation analysis of miR-126 and EGFL7 in HCC tissues. [score:1]
HEPG2 cells in logarithmic phase were seeded into 96-well plates, and co -transfected with EGFL7-3′UTR-WT and miR-126 mimic plasmids (EGFL7-3′UTR-WT + miR-126) using Lipofectamine 2000 when the cell density was about 70%. [score:1]
Our study aims to explore the potential mechanism of miR-126 affecting cell proliferation, apoptosis, and angiogenesis in HCC via mediating EGFL7 and the ERK signaling pathway. [score:1]
MiR-126 is situated in an intron of EGFL7, and miR-126 could be generated by 3 different transcripts on EGFL7 [15]. [score:1]
The fragment of EGFL7 gene containing miR-126 binding sites in 3′-UTR region was inserted into dual-luciferase reporter vector to construct recombinant wild-type plasmid (EGFL7-3′UTR-WT) and mutant-type plasmid (EGFL7-3′UTR-MUT). [score:1]
HepG2 cells were co -transfected with EGFL7-3′UTR-WT and miR-126 mimic plasmids. [score:1]
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2
[+] score: 325
Other miRNAs from this paper: rno-mir-21, rno-mir-27a, rno-mir-126a, rno-mir-127
Overexpression of miR-126 by a lentiviral vector (lenti-miR-126) was found to downregulate the mRNA expression of mesenchymal cell markers (α-SMA, sm22-a, and myocardin) and to maintain the mRNA expression of progenitor cell markers (CD34, CD133). [score:10]
In the animal mo del of mice and zebra fish, the loss-of-function study by deleting the targeted miR-126 gene leads to loss of vascular integrity during development and then result in defective angiogenesis[16][17] Additional study has demonstrated that miR-126 can positively regulate the response of ECs to vascular endothelial growth factor (VEGF), and improve angiogenesis in part by directly repressing negative regulators of the VEGF pathway, through mechanism involving the sprouty-related protein 1 (SPRED1) and phosphoinositol-3 kinase regulatory subunit 2 (PIK3R2)[18]. [score:8]
This conclude that miR126 inhibits EndMT in EPCs by down -regulating the direct target gene of PIK3R2. [score:7]
In the cellular process of EndMT, there was an increase in the protein expression of PIK3R2 and the nuclear transcription factors FoxO3 and Smad4; PI3K and phosphor-Akt expression decreased, a change that was reversed markedly by overexpression of miR-126. [score:7]
To explore the mechanisms of miR-126 in the regulation of EPC EndMT, we confirmed that the gene coding for PI3K regulatory subunit p85 beta (PIK3R2), a target gene of miR-126 identified previously in endothelial cells [16], is also the target gene of miR-126 in EPCs by using a luciferase reporter assay, consistent with the findings in circulating EPCs in preeclampsia[25]. [score:6]
To demonstrate that PIK3R2 is the target gene of miR-126 during EndMT process in EPCs, we performed the loss-of-function experiment by knocking down PIK3R2 gene expression level to mimic the same effect of miR-126 on EPCs (Figure 4). [score:6]
In addition, we found that miR-126 interacts with its target gene PIK3R2 to inhibit the EndMT process, involving regulation of the PI3K/Akt-FoxO3/Smad4 signalling pathway. [score:6]
These results show that miR-126 targets PIK3R2 to inhibit EPC EndMT and that this process involves regulation of the PI3K/Akt signalling pathway. [score:6]
TGFβ1 treatment markedly decreased the mRNA expression of progenitor cell markers (CD34, CD31, CD133, and KDR) and endothelial cell markers (VEGF, Flt-1, eNOS, and iNOS), while overexpression of miR-126 increased the mRNA expression of the corresponding markers compared to the miR-126 control (Figure 2A & 2B). [score:6]
miR-126/miR-126* expression is downregulated in cancer cells by promoter methylation of their host gene Egfl7[13]. [score:6]
Furthermore, knockdown of PIK3R2 gene expression level showed reversed morphological changes of the EPCs treated with TGFβ1, thereby giving the evidence that PIK3R2 is the target gene of miR-126 during EndMT process. [score:6]
miR-126 inhibits EPC EndMT via targeting PIK3R2. [score:5]
Taken together, these findings imply that miR-126 inhibited EPC EndMT via targeting PIk3R2 to enhance PI3K/Akt activation. [score:5]
In addition, miR-126 expression was simultaneously downregulated by the TGFβ1 (5 ng/mL) treatment for 7 days compared to the normal control (Figure 1D). [score:5]
Overexpression of miR-126 inhibited the EndMT process of EPCs induced by TGFβ1. [score:5]
Furthermore, overexpression of miR-126 could be a potential therapy for pulmonary vascular intima hyperplasia in pulmonary hypertension, a challenging disease in medicine. [score:5]
As a result of miR-126 overexpression in EPCs undergoing the EndMT process, we observed the diminished mRNA expression of mesenchymal cell markers, such as αSMA, sm22, and myocardin. [score:5]
Overexpression of miR-126 inhibits TGFβ1 -induced EndMT of EPCs. [score:5]
These results suggest that miR-126 regulates the EndMT process via the direct target gene of PIK3R2, and involves the PI3K-Akt signaling pathways. [score:5]
Taken together, our findings imply that miR-126 decreases PIk3R2 expression to enhance PI3K/Akt activation, thereby inhibiting EndMT in EPCs. [score:5]
Cytoplasmic expression of αSMA in EPCs treated with TGFβ1 was inhibited markedly by miR-126. [score:5]
After treatment of EPCs with TGFβ1 (5 ng/mL) for 7 days, we found that the mRNA expression level of Egfl7 did not alter while miR-126 expression level decreased gradually along the 7 day treatment course (Figure S3). [score:5]
In summary, we found that overexpression of miR-126 inhibited EndMT of EPCs. [score:5]
Next, we demonstrated that overexpression of miR-126 had no effect of expression level of its host gene Egfl7 (. [score:5]
After an extensive review of online microRNA database by using TargetScan, picTar and RNA22, we selected PIK3R2 as a putative target gene of miR-126 in EPCs. [score:5]
miR-126 has the potential to be used as a biomarker for the early diagnosis of intimal hyperplasia in cardiovascular disease and can even be a therapeutic tool for treating cardiovascular diseases mediated by the EndMT process. [score:5]
Given our current results that overexpression of miR-126 enhanced the level of phosphor-Akt, our findings indicate that miR-126 might promote PI3K/Akt activation to negatively regulate the FoxO3/Smad4 signalling pathway. [score:4]
In this study, miR-126 inhibited EPC EndMT, accompanied by a significant decrease in nuclear FoxO3 and Smad4 levels, suggesting a role of the FoxO3/Smad4 complex in the negative regulation of miR-126 in EPC EndMT. [score:4]
PIK3R2 is a direct target of miR-126 in EPCs. [score:4]
After treatment with TGFβ1 (5 ng/mL) for 7 days, we examined morphological changes as well as gene expression profile as described in Figure 1 and 2. We found that knockdown of PIK3R2 significantly reversed the morphological changes of EPCs from cobblestone-like to spindle-shape appearance in the presence of TGFβ1, similar to the findings observed in the lenti-miR-126 treated EPCs (Figure 4B). [score:4]
Next, we investigated if PIK3R2 is the target gene regulated by miR-126 to inhibit the EndMT process in EPCs. [score:4]
Consistent with overexpression of miR-126 in EPCs, we found that PIK3R2 knockdown had similar effect to block TGFβ1 induced EndMT process. [score:4]
The mechanism of miR-126 downregulation by TGFβ1 is prabobaly through the Egfl7 T-2 promoter containing CpG islands. [score:4]
It remains unclear whether miR-126 inhibition of the EndMT process is indirectly controlled by decreasing the secretion of TGFβ1 from EPCs undergoing EndMT. [score:4]
The luciferase reporter assay showed that the PI3K regulatory subunit p85 beta (PIK3R2) was a direct target of miR-126 in EPCs. [score:4]
In vascular endothelial cells, miR-126 could negatively regulate the PI3K/Akt signalling pathway by targeting PIK3R2 [16]. [score:4]
Recent studies have demonstrated that the gene coding for the phosphoinositide 3-kinase (PI3K) regulatory subunit p85 beta (PIK3R2) is one of the targets of miR-126 [19]. [score:4]
PIK3R2 was a direct target of miR-126 in EPCs. [score:4]
These results led us to hypothesize that miR-126 targets PIK3R2 to facilitate PI3K/Akt activation and then to negatively modulate the Smad2/3 -dependent signalling pathway to repress the EPC EndMT process. [score:3]
Here, our experiments show that deficiency of miR-126 expression is, at least in part, responsible for the EndMT of EPCs induced by TGFβ1. [score:3]
EPCs induced by TGFβ1 were transfected with a miR-126 -expressing lentiviral vector, an empty vector (lentivector), or neither, and EPCs without any treatment were used as the normal control. [score:3]
To further confirm the role of miR-126 in EPC EndMT, overexpression of miR-126 was achieved in EPCs by transfection with a lentivirus vector encoding miR-126. [score:3]
In the present study, phosphor-Akt levels decreased markedly in TGFβ1 -treated EPCs, whereas levels increased notably by overexpression of miR-126. [score:3]
Overall, overexpression of miR-126 partially reversed the TGFβ1 -induced EndMT process in EPCs. [score:3]
miR-126 expression decreases in EPC EndMT. [score:3]
Notably, in our study, miR-126 was found to inhibit the decrease in mRNA levels of the progenitor cell markers, CD133 and CD34, implying an important role for miR-126 in maintaining the EPCs progenitor properties. [score:3]
After the treatment with TGFβ1 (5 ng/mL) for 7 days, EPCs underwent a morphological change from a cobblestone-like to a spindle-shaped appearance, while overexpression of miR-126 partially reversed the morphological changes (Figure 1B). [score:3]
However, we do understand that the only way to reveal all other possible target genes is to study the mRNA microarray data from EPCs infected with lenti-miR-126. [score:3]
miR-126 activated the PI3K/Akt and inhibited the FoxO3/Smad4 signalling pathways in TGFβ1 -induced EPCs. [score:3]
To explore the role of miR-126 in TGFβ1 -induced EndMT of EPCs, EPCs were transfected with a lentiviral vector (lenti-miR-126) to overexpress endogenous miR-126, and an empty control lentiviral vector was used as a control (marked as lenti-miR control). [score:3]
Figure S3 miR-126 on Egfl7 expression in EPC EndMT. [score:3]
The Expression plasmids for miR-126 was created using PCR amplification with rat genomic DNA as templates. [score:3]
0083294.g003 Figure 3(A) Diagram of PIK3R2-3′UTR-containing luciferase reporter gene construct and the 22-bp target site of miR-126 in PIK3R2-3′UTR. [score:3]
Our research provides a tool to deliver vector -based miR-126 to an endothelial system, thereby inhibiting intimal hyperplasia through the EndMT mechanism. [score:3]
The infection efficiency of lenti-miR-126 was 87.56%, and endogenous miR-126 expression in lenti-miR126 transfected EPCs was 3.6-fold higher than that in the control (Figure S1). [score:3]
EPCs or miR-126 overexpressing EPCs were then transfected with the wt or mt 3′UTR vector. [score:3]
In addition, we determined the impact of miR-126 on PIK3R2 in EPCs and TGFβ1 -treated EPCs since both mRNA and protein expression levels of PIK3R2 significantly decreased (Figure 3C & 3D). [score:3]
MIMAT0000444), the partner to miR-126 that is derived from the same transcript within Egfl7 gene, had a similar expression pattern in EPCs when treated with TGFβ1 for 7 days course (Figure S3A). [score:3]
These results demonstrated that miR-126 inhibited the EndMT process of EPCs. [score:3]
In details, we transfected EPCs with lenti-miR-126 in the presence or absence of LY294002, a potential inhibitor of PIK3. [score:3]
However, in the lentiviral miR-126 treated EPCs, we did not observe any mRNA expression level changes of Egfl17 (Figure S3A). [score:3]
Microarray -based expression profiles in our previous study have identified several miRNAs in EPCs, such as microRNA 21 (miR-21), microRNA 27a (miR-27a), and microRNA 126 (miR-126) [9]. [score:3]
EPCs were treated with TGFβ1 (5 ng/mL) for 1, 3, 5 and 7 days, and miR-126 relative expression was detected by using quantitative real time-PCR (qRT-PCR). [score:3]
miR-126 expression was depressed in the process of EPC EndMT. [score:3]
When EPCs were treated with TGFβ1, the protein levels of PI3K and phosphor-Akt decreased noticeably, which were partially reversed to basal levels by overexpression of miR-126 (Figure 5) and not by the miR-126 empty vector. [score:3]
Endogenous miR-126 expression in lenti-miR-126 -transfected EPCs increased to 3.6 times compared with the vehicle control by using quantitative real time-PCR (C). [score:2]
Additionally, we found that PIK3R2 protein levels were increased markedly in TGFβ1 -treated EPCs and that levels were significantly decreased by miR-126, suggesting that PIK3R2 was involved in the negative regulation of miR-126 in EPC EndMT. [score:2]
miR-126, an endothelial-specific miRNA enriched in EPCs, regulates EPC proliferation, mobilization, and migration [9, 14]. [score:2]
In addition, the characteristic decreased α-SMA gene expression profiles followed the similar pattern of changes between lenti-miR-126 treated and knockdown of PIK3R2 group in EPCs (Figure 4B). [score:2]
MicroRNA-126 is located within 7the intron of epidermal growth factor-like domain 7 (Egfl7) and is highly expressed in vascular endothelial cells [12]. [score:2]
miR-126 regulates PI3K/Akt signalling pathways involved in TGFβ1 -induced EndMT of EPCs. [score:2]
In addition, it will be interesting to explore whether the PI3K/Akt/FoxO3 signalling pathway, under the regulation of miR-126, would be involved in homeostasis of EPCs. [score:2]
The physiological significance of miR-126 and Egfl7 is distinct as demonstrated knockout mice mo del[24]. [score:2]
Analyses of mRNA levels for mesenchymal markers (α -SMA, sm22-α, and myocardin) showed that the expression levels of mesenchymal-derived markers were increased only by TGFβ1, while they were decreased in the presence of both miR-126 and TGFβ1 compared to the miR-126 control (Figure 2C). [score:2]
miR-126 regulates Smad4/FoxO3 signalling pathways involved in TGFβ1 -induced EndMT of EPCs. [score:2]
Therefore, future research will be needed to investigate other interesting target genes or pathways regulated by miR-126 in EPCs. [score:2]
However, the role of miR-126 in regulating the transition of EPCs to mesenchymal cells has not been reported to date. [score:2]
The inconsistency might be due to the different times of TGFβ1 stimulus, and it might also result from the disparity in basal levels of miR-126 between circulating EPCs and BM-derived EPCs, which should be explored further. [score:1]
miR-126* (miRBase accession no. [score:1]
These results are consistent with the previous findings in mesenchymal stem cells that miR-126 induced phosphorylation of Akt without exogenous stimulus [27]. [score:1]
In the present study, we assessed the effects of miR-126 on TGFβ1 -induced EndMT of EPCs isolated from the bone marrow (BM). [score:1]
MIMAT0000444), the partner to miR-126 that is derived from the same precursor transcript within the Egfl7 ghen, forms a miRNA pair with miR-126 to exert physiological functions. [score:1]
MiR-126, but not the miR-126 empty vector decreased the protein levels of FoxO3 and Smad4 in TGF-β1 -treated EPCs (Figure 5). [score:1]
TGFβ1 may induce hypermethylation in T-2 promoter which in turn silences intronic miR-126 located within the 7th intron of the host Eglf7 gene. [score:1]
Future research should be focused on investigating the diagnostic and therapeutic values of miR-126 in those cardiovascular diseases. [score:1]
By using flow cytometry analysis, the transfection efficiency of lenti-miR-126 and lenti-GFP reached 87.56% and 90.91% respectively (B). [score:1]
U6 snRNA (for miR-126) and β-actin (for mRNAs) were used as endogenous controls. [score:1]
Studies have shown that miR-126 does not affect the differentiation of EPCs into mature endothelial cells [9], although it favours the proliferation, mobilization, and migration of EPCs [14, 15]. [score:1]
In the present study, miR-126 levels decreased significantly in the EPC EndMT induced by TGFβ1, suggesting that miR-126 could be involved in the EndMT process of EPCs. [score:1]
Cells were then transfected with the PIK3R2 3′UTR wild type (wt) plasmid or the PIK3R2 3′UTR mutant (mt) plasmid in the presence of either miR-126 or miR-control. [score:1]
These results indicate that PIK3R2 is involved in the EndMT mechanism of miR-126 in EPCs. [score:1]
A miR-126 F 5'-GCTGTCAGTTTGTCAAATAC-3' R 5'-GTGCAGGGTCCGAGGT-3' B miR-126* F 5’-GGGCATTATTACTTTTGG-3’ R 5’- TGCGTGTCGTGGAGTC-3’ C U6 F 5'-CTCGCTTCGGCAGCACA-3' R 5'-AACGCTTCACGAATTTGCGT-3' D CD31 F 5'-AGTCAGTAAATGGGACTGCACCCA-3' R 5'-TCTCTGGTGGGCTTGTCTGTGAAT-3' E CD34 F 5'-AGACTCAGGGAAAGGCCAATGTGA-3' R 5'-GCCACCACATGTTGTCTTGCTGAA-3' F CD133 F 5'-AACGTGGTCCAGCCGAATG-3' R 5'-TCCCAGGATGGCGCAGATA-3' G KDR F 5'-AGTGGCTAAGGGCATGGAGTTCTT-3' R 5'-GGGCCAAGCCAAAGTCACAGATTT-3' H α-SMA F 5'-AATATTCTGTCTGGATCGGCGGCT-3' R 5'-GAAGCATTTGCGGTGGACAATGGA-3' I sm22-α F 5'-AAGATATGGCAGCAGTGCAGAGGA-3' R 5'-CCATTTGAAGGCCAATGACGTGCT-3' J myocardin F 5'-ACGGGATGGAGGTTTCTGTGACAA-3' R 5'-GGCACATTTCGAATGCATCACCGA-3' K VEGF F 5'-TCACCAAAGCCAGCACATAGGAGA-3' R 5'-TTTCTCCGCTCTGAACAAGGCTCA-3' L Flt-1 F 5'-TAGATGTCCAAATAAGCCCGCCGA-3' R 5'-TCAATCCGCTGCCTGATAGATGCT-3' M eNOS F 5'-TATTTGATGCTCGGGACTGCAGGA-3' R 5'-ACGAAGATTGCCTCGGTTTGTTGC-3' N iNOS F 5'-TGATCTTGTGCTGGAGGTGACCAT-3' R 5'-TGTAGCGCTGTGTGTCACAGAAGT-3' O β-actin F 5'-AGCACAGAGCCTCGCCTTTG-3' R 5'-ACATGCCGGAGCCGTTGT-3' P PIK3R2 F 5'-GCACCACGAGGAACGCACTT-3' R 5'-CGTCCACTACCACGGAGCAG-3' Q Egfl7 F 5’-CTCTCCTACCCACAGCAATATG-3’ R 5’-CCTCTCCTGTACTGCATTCATC-3’ Total RNA was extracted using Trizol reagent (Invitrogen) according to the manufacturer’s instructions. [score:1]
The construct of miR-126 was confirmed by sequencing. [score:1]
One of the endothelial-specific microRNAs is miR-126 (miRBase accession no. [score:1]
The luciferase-3′-UTR reporter plasmid containing a PIK3R2 3′-UTR carrying a putative or a mutant miR-126 binding site was constructed and cloned downstream of a cytomegalovirus (CMV) promoter -driven firefly luciferase cassette in a pCDNA3.0 vector. [score:1]
This study aimed to explore the role of microRNA 126 (miR-126) in the endothelial-to-mesenchymal transition (EndMT) induced by transforming growth factor beta 1 (TGFβ1). [score:1]
Immunofluorescence staining showed that the α-SMA protein was synthesized in the cytoplasm of EPCs treated with TGFβ1; however, the cytoplasmic levels of α-SMA were significantly lowered by miR-126 (Figure 2D). [score:1]
To investigate whether if miR-126/miR-126* host gene Egfl7 could also be involved the mechanism of EndMT in EPCs, quatitative real-time PCR did not show any difference of Egfl7 mRNA expression in the presence of TGFβ1 (. [score:1]
EPCs were transfected with lenti-miR-126 and lenti-GFP (MOI = 10) for 48 hours, and the transfection efficiency was detected by immunofluorescence (A). [score:1]
They used selectively floxed Egfl7 (Delta) and miR-126 (Delta) alleles to reveal that Egfl7 (Delta/Delta) mice were phenotypically normal, whereas miR-126 (Delta/Delta) mice bearing a 289-nt micro deletion recapitulated previously described Egfl7 embryonic and postnatal retinal vascular phenotypes. [score:1]
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As shown in Figure 3A, miR-126-3p overexpression and inhibition were, respectively, responsible for downregulation (0.47- and 0.51-fold; P < 0.001) and upregulation (1.14- and 1.67-fold; P < 0.001) of the PIK3R2 and SPRED-1 mRNA levels. [score:11]
Overexpression of miR-126-3p by agomir inhibited neointimal formation in HSV organ cultures ex vivoBased on our clinical findings and in vitro results indicating the beneficial effects of miR-126-3p on HSVEC proliferation and migration, we hypothesized that overexpression of miR-126-3p by agomir could inhibit neointimal hyperplasia by accelerating reendothelialization in a well validated ex vivo organ culture mo del of HSV. [score:9]
Figure 3(A) Overexpression and inhibition of miR-126-3p, respectively, promoted and inhibited PIK3R2 and SPRED-1 mRNA levels in HSVECs. [score:7]
Moreover, it is possible to manipulate miR-126-3p expression and observe changes in target gene expression by the agomir method. [score:7]
As it known to all that CABG provides a practical opportunity for the local delivery of agents that can regulate the pathophysiology of autologous vein graft restenosis inside the operating room, we propose that the upregulation of miR-126-3p levels in a rat vein arterialization mo del at the time of engraftment through ex vivo treatment of the venous wall is a clinically acceptable administration method that could lead to localized manipulation of the target miRNA. [score:7]
indicated that local delivery of the miR-126-3p agomir resulted in significantly downregulated protein levels of PIK3R2 and SPRED-1 at 7 days after surgery (Figure 6A and 6B), which also supported that the local delivery of miR-126-3p agomir prior to implantation was efficient and that PIK3R2 and SPRED-1 were indeed target genes of miR-126-3p in vivo. [score:6]
Taken together, these results implied that overexpression of miR-126-3p by agomir in HSVECs promoted proliferation and migration mediated, at least in part, by the regulation of ERK1/2 and AKT signaling through SPRED-1 and PIK3R2 targeting. [score:6]
Our results strengthen hypothesis that local delivery of miR-126-3p by agomir at the time of engraftment is sufficient to bind target sequences and suppress neointimal formation in vein grafts in vivo. [score:5]
Overexpression of miR-126-3p resulted in an increased proliferation rate, whereas inhibition of miR-126-3p had the opposite effect (Figure 2D). [score:5]
Overexpression of miR-126-3p by agomir inhibited neointimal formation in HSV organ cultures ex vivo. [score:5]
Figure 1(A) Circulating miR-126-3p expression was detected by real-time PCR in human plasma samples from healthy controls and patients with complex multi-vessel coronary artery disease prepping for a CABG. [score:5]
Based on our clinical findings and in vitro results indicating the beneficial effects of miR-126-3p on HSVEC proliferation and migration, we hypothesized that overexpression of miR-126-3p by agomir could inhibit neointimal hyperplasia by accelerating reendothelialization in a well validated ex vivo organ culture mo del of HSV. [score:5]
Recent research has provided evidence that miR-126-3p NP-conjugated stents significantly inhibit the development of neointimal hyperplasia in a rabbit mo del of endothelial denudation of the iliac artery [27]. [score:4]
PIK3R2 and SPRED-1 protein levels were significantly downregulated by local delivery of the miR-126-3p agomir at 7 days after transfection. [score:4]
miR-126-3p had no effect on HSVSMC proliferation and migration in vitroTo examine the side effects of dysregulated miR-126-3p expression in SMCs of vein grafts, primary HSVSMCs were isolated and identified (Supplementary Figure 3). [score:4]
Therapeutic upregulation of miR-126-3p by agomir attenuated vein graft neointimal formation in vivoHistomorphometric analysis was performed at 4 weeks after venous implantation (Figure 7A–7D). [score:4]
Among the verified targets of miR-126-3p, PIK3R2 and SPRED-1 are known as negative regulators of the VEGF signaling pathway to critically influence proliferation and migration in human umbilical vein endothelial cells (HUVECs) [24]. [score:4]
To examine the side effects of dysregulated miR-126-3p expression in SMCs of vein grafts, primary HSVSMCs were isolated and identified (Supplementary Figure 3). [score:4]
Among the verified targets of miR-126-3p, SPRED-1and PIK3R2 are known as negative regulators of the VEGF (vascular endothelial growth factor) signaling pathway to critically influence proliferation and migration in human umbilical vein endothelial cells (HUVECs) [24]. [score:4]
Therapeutic upregulation of miR-126-3p by agomir attenuated vein graft neointimal formation in vivo. [score:4]
We found that circulating miR-126-3p levels in patients undergoing CABG showed a brief rise during the perioperative period, which increased one day after surgery, peaked at 3 day after surgery, remained up-regulated at 7 days after surgery, and then gradually declined to baseline at 14 days after surgery (Figure 1B, P < 0.05). [score:4]
Studies have shown that the upregulation of EC-specific miR-126-3p by agomir has no influence on basal HSVSMC migration (Figure 4E–4F). [score:4]
Although miR-126-3p was still up-regulated at 14 days, there were no significant differences compared with those that were not cultured. [score:3]
miR-126-3p overexpression limited neointimal formation of vein grafts in vivo. [score:3]
Two different groups confirmed that Ad -mediated overexpression of miR-126-3p and endothelial microparticle -mediated transfer of miR-126-3p in balloon-injured arteries promoted reendothelialization in arterial balloon injury mo dels [26, 28]. [score:3]
However, even the peak value remained far below the levels of miR-126-3p expression in normal people (Figure 1C, P < 0.01). [score:3]
Effect of miR-126- 3p overexpressionon adult HSVEC proliferation and migration in vitro. [score:3]
To further validate the relevance of miR-126-3p in CABG, we assessed dynamic changes in plasma miR-126-3p expression in patients undergoing CABG at different time points during the perioperative period. [score:3]
To the best of our knowledge, this is the first report to demonstrate that miR-126-3p exerts a vasculoprotective role in the setting of vein graft disease. [score:3]
Relative expression levels miR-126-3p in plasma from CABG patients and vein graft mo del. [score:3]
We established a rat vein arterialization mo del and adopted local overexpression of miR-126-3p in vein bypass grafts prior to implantation using a “cuff” anastomotic technique (Supplementary Figure 5). [score:3]
In the present study, our results showed that miR-126-3p overexpression in the rat vein grafts accelerated reendothelialization. [score:3]
Consistent with these findings, the expression of both PIK3R2 and SPRED-1 proteins in HSVECs was significantly decreased upon treatment with the miR-126-3p agomir and was significantly increased upon transfection with the miR-126-3p antagomir (Figure 3B and 3C). [score:3]
Overexpression of miR-126-3p by agomir improved reendothelialization in vivoWe sought to determine whether the beneficial effects of the miR-126-3p agomir were associated with improved reendothelialization in the vein grafts. [score:3]
Unexpectedly, but within our understanding, we found that overexpression of the miR-126-3p by agomir had no effect on migration and proliferation in HSVSMCs. [score:3]
Using this mo del, we have demonstrated that miR-126-3p expression can be effectively manipulated by agomir to accelerate reendothelialization and reduce neointimal hyperplasia in clinically relevant vein grafts. [score:3]
We newly confirmed that miR126-3p targets SPRED-1 and PIK3R2 and activates the ERK1/2 and AKT signaling pathways in HSVECs. [score:3]
Overexpression of miR-126-3p by agomir improved reendothelialization in vivo. [score:3]
The roles of miR-126-3p are often discussed in the context of a number of vascular diseases including myocardial infarction, diabetic vascular complications, pulmonary arterial hypertension, and ischemic stroke [20– 23]. [score:3]
By contrast, Zhou et al. reported that systemic depletion of miR-126-3p in mice inhibited neointimal lesion formation of carotid arteries induced by cessation of blood flow [43]. [score:3]
Hence, we considered worth to further investigating dysregulated miR-126-3p expression on migration and proliferation in HSVSMCs before moving to translational studies. [score:3]
There is a growing body of evidence suggesting that miR-126-3p may play a vasculoprotective role in vein graft disease [24– 28]. [score:3]
Altered miR-126-3p expression in patients with CAD after CABG. [score:3]
miR-126-3p targeted PIK3R2 and SPRED-1 and activated the ERK1/2 and AKT signaling pathways in HSVECs. [score:3]
The levels of two target genes were altered after miR-126-3p treatment. [score:3]
Jansen et al. found that intercellular transfer of miR-126-3p reduces arterial SMC proliferation and migration, which was contrasted with the experimental results that decreased expression of miR-126-3p led to increased proliferation of arterial SMCs by Zhou et al [27, 42, 43]. [score:3]
Loss-of-function studies were not performed in this part of the analysis because no previous evidence have suggested that miR-126-3p is endogenously expressed in VSMCs. [score:3]
To our knowledge, only a few in vivo studies have attempted to illuminate the role of miR-126-3p in the development of intimal hyperplasia in various vessels, and none have studied vein grafts. [score:2]
Recently, miR-126-3p has emerged as irreplaceable endothelial cell–restricted miRNA that is involved in the regulation of vascular integrity and angiogenic signaling [18, 19]. [score:2]
Compared with healthy subjects, all preoperative patients had a significantly lower level of miR-126-3p expression (Figure 1A, P < 0.0001). [score:2]
In the present work, we compared the expression levels of miR-126-3p in patients with CAD before and after CABG. [score:2]
In our study, all of these severe CAD patients who were preparing for CABG had a significantly lower level of miR-126-3p expression compared with the healthy subjects. [score:2]
To further test this assumption, we established a HSV organ culture mo del to validate the role of miR-126-3p in neointimal formation of vein grafts. [score:1]
This result is consistent with previous reports showing that the function of EC-specific miR-126-3p on cell migration and proliferation is cell type-specific [28]. [score:1]
In general, the changes in miR-126-3p in HSV were almost consistent with the findings obtained for human plasma. [score:1]
In summary, we have demonstrated that miR-126-3p promotes proliferation and migration in HSVECs and that transfection of the miR-126-3p agomir significantly improves reendothelialization and thus prevents neointimal formation of the vein graft ex vivo and in vivo. [score:1]
HSVECs were transfected with 100 nmol miR-126-3p agomir and antagomir. [score:1]
n = 6. [#] P < 0.001 vs uncultured vein, * P < 0.01 vs NC agomir -treated and miR-126-3p agomir -treated veins. [score:1]
Fluorescent staining showed that local application of the miR-126-3p agomir was effective, long-lasting, and restricted to the conduit, and it did not affect other organs. [score:1]
Figure 6Exogenous miR-126-3p improved blood flow in vein grafts in vivo(A) Representative western blots and quantification (B) of PIK3R2 and SPRED-1 proteins are shown. [score:1]
Several groups have revealed that miR-126-3p levels are low in the serum of stable CAD patients, and there is a positive association between circulating miR-126 and myocardial infarction [20, 38]. [score:1]
Moreover, immunohistochemical staining of α-SMA demonstrated the presence of abundant SMCs localized in the neointima in vein grafts, and the accumulation of positively stained SMCs was markedly reduced in vein grafts treated with miR-126-3p agomir (22160 ± 2271 mm [2] vs 33832 ± 4735 mm [2] and 35468 ± 1803 mm [2], respectively, P both < 0.05, Figure 7G). [score:1]
Luminal staining for Evans blue indicated that reendothelialization was significantly greater in the miR-126-3p agomir group in comparison with the NC agomir group and vein graft group (86% ± 4.19% vs. [score:1]
We sought to determine whether the beneficial effects of the miR-126-3p agomir were associated with improved reendothelialization in the vein grafts. [score:1]
Interestingly, miR-126-3p has emerged as a controversial miR involved in SMC proliferation and migration. [score:1]
Hematoxylin eosin staining revealed that treatment with miR-126-3p agomir dramatically reduced neointimal thickness, whereas treatment with NC agomir and no treatment resulted in a dramatically increased neointima (56.83 ± 9.99 μm vs 141.7 ± 13.12 μm and 127.3 ± 16.64 μm, respectively, P both < 0.01, Figure 7A and 7E). [score:1]
Finally, we generated an inflammatory cytokine -induced inflammation mo del in vitro [30], in which HSVSMCs were cultured with tumor necrosis factor-α (TNF-α, 10 ng/ml) and increasing concentrations of miR-126-3p agomir for the tested functions. [score:1]
miR-126-3p agomir and miR-126-3p antagomir were obtained from RiboBio (Guangzhou, China) and transfected into cells using riboFECTTM CP transfection reagent (RiboBio) according to the manufacturer’s protocol. [score:1]
We also established the ex vivo HSV culture mo del and rat vein grafting mo del to better assess whether a single delivery of miR-126-3p agomir would be sufficient to reduce intimal hyperplasia of the vein graft. [score:1]
Effect of miR-126- 3p overexpressionon adult HSVEC proliferation and migration in vitroTo investigate the function of miR-126-3p in vein graft cells and provide evidence for further applications, we successfully isolated and identified primary HSVECs from patients undergoing CABG surgery (Supplementary Figure 1). [score:1]
As shown in Supplementary Figure 6, transfected vein grafts showed broadly apparent Cy3 staining throughout the vessel wall under fluorescent light at 24 hours after Cy3-labeled miR-126-3p agomir transfection, and it was still detectable after 7 days. [score:1]
Effect of the miR-126-3p agomir on the human saphenous vein organ culture mo del. [score:1]
Here, for the first time, we identified the role of miR-126-3p in the proliferation and migration of HSVECs using gain- and loss-of-function studies. [score:1]
Taken together, these data demonstrated that the effect of miR-126-3p on cell migration and proliferation is cell type-specific and that the miR-126-3p agomir had no effect on HSVSMC proliferation and migration. [score:1]
Given the controversial results present in various mo dels, we aimed to clarify the effects of the miR-126-3p agomir in an established rat vein arterialization mo del as described [48, 49]. [score:1]
Olivieri, F. et al. demonstrated that plasma loss of endothelial miR-126-3p in patients with type 2 diabetes is associated with diabetic vascular complications [21]. [score:1]
In the present study, the miR-126-3p agomir was used because of its excellent prospects in clinical applications relative to viral vectors. [score:1]
Notably, HSVEC treatment with miR-126-3p agomir resulted in increased ERK1/2 and AKT phosphorylation, whereas transfection with the miR-126-3p antagomir had the opposite effect (Figure 3D). [score:1]
The Masson trichrome staining showed that the percentage of neointimal area occupied by blue-colored fibers (collagen) did not obviously differ between the miR-126-3p agomir -treated group and the other control groups (P > 0.05, Figure 7F). [score:1]
In two of the three cultured segments, miR-126-3p agomir and miR-126-3p negative control agomir (NC agomir) were transfected for the initial culture; the remaining segment received no treatment (untreated control). [score:1]
To investigate the role of miR-126-3p in the clinical setting of vein graft disease, we first evaluated the expression of plasma miR-126-3p in CAD patients by preparing CABG and healthy volunteers from the medical examination center of our hospital by qRT-PCR. [score:1]
Thus, we hypothesize that the transient change in circulating miR-126-3p in CABG surgery may reflect early compensatory mechanism by which endothelial cell function is maintained in vein grafts, but this compensation is incomplete. [score:1]
Thus, we tested the transfection efficiency by using a Cy3-labeled miR-126-3p agomir, and visualized the results using a fluorescence microscope. [score:1]
miR-126-3p agomir had no effect on HSVSMC proliferation and migration in vitro. [score:1]
To explore the effect of the miR-126-3p agomir in HSV organ culture, four equal individual segments were created for each leftover HSV, one segment (uncultured control) was immediately formalin-fixed, and the remaining segments were cultured in complete medium. [score:1]
Whether miR-126-3p could be used as an intervention to prevent vein graft failure remains uncertain. [score:1]
Local delivery of miR-126-3p agomir improved blood flow in vivo in a rat vein grafting mo del. [score:1]
Taken together, these data suggested that miR-126-3p participates in HSVEC proliferation and migration and that agomir treatment is a viable gene strategy to increase miR-126-3p functions in HSVECs. [score:1]
The luminal diameter of vein grafts either in the NC agomir group or vein graft group was thinner than that in the miR-126-3p agomir treated group (2.08 ± 0.14 mm and 2.07 ± 0.07 mm vs. [score:1]
This idea is supported by a previous report that miR-126-3p was released from activated endothelial cells by apoptotic bodies and served as a compensatory signal to confer atheroprotection in atherosclerosis [39]. [score:1]
All these results demonstrated that, consistent with observations ex vivo, the miR-126-3p agomir delivery locally accelerates reendothelialization after venous implantation and thereby attenuates vein graft luminal stenosis and neointimal formation. [score:1]
Local delivery of miR-126-3p agomir improved blood flow in vivo in a rat vein grafting mo delOwing to the limitations of the ex vivo mo del, we performed further experiments to test the feasibility of applying miR-126-3p agomir in vivo and provide a practical basis for further clinical application. [score:1]
At 24 h after Cy3-labeled miR-126-3p agomir transfection in HSVECs, specific red fluorescence could be detected within the cytoplasm at concentrations ranging from 25 to 200 nmol (Supplementary Figure 2). [score:1]
Owing to the limitations of the ex vivo mo del, we performed further experiments to test the feasibility of applying miR-126-3p agomir in vivo and provide a practical basis for further clinical application. [score:1]
To test this hypothesis and confirm the previous results, cultured HSVECs were transfected with either miR-126-3p agomir or miR-126-3p antagomir. [score:1]
The ultimate goal of our study was to investigate the role of miR-126-3p in vein graft disease and the value of the miR-126-3p agomir as a future gene therapy in CABG. [score:1]
Four groups were created after grafting: (1) normal vein group, n = 21; (2) vein graft group (vein grafted to the abdominal aorta without transfection), n = 21; (3) miR-126-3p negative control agomir group (NC agomir group, vein grafts treated with miR-126-3p negative control agomir), n = 21; (4) miR-126-3p agomir group (vein grafts treated with miR-126-3p agomir), n = 27. [score:1]
miR-126-3p agomir promoted reendothelialization in vivo. [score:1]
Our results established the basic clues demonstrating that miR-126-3p participates in CABG. [score:1]
Moreover, we found that circulating miR-126-3p levels showed a brief rise in the perioperative period. [score:1]
HSVECs were transfected with miR-126-3p agomir, miR-126-3p negative control agomir (NC agomir), miR-126-3p antagomir and miR-126-3p negative control antagomir (NC antagomir). [score:1]
Quantitative analysis of immunopositive cells in the lumen of vein grafts revealed that reendothelialization was significantly increased in the miR-126-3p agomir group and reached 85% by day 14. [score:1]
miR-126-3p had no effect on HSVSMC proliferation and migration in vitro. [score:1]
Circulating miR-126-3p levels were continuously detected by qRT-PCR 1 day prior to surgery and at 1, 3, 7 and 14 days after CABG. [score:1]
Figure 2HSVECs were transfected with 100 nmol miR-126-3p agomir and antagomir. [score:1]
During surgery, 5 nmol miR-126-3p agomir or miR-126-3p negative control agomir (NC agomir), dissolved in normal saline (0.9%) according to the manufacturer’s instructions, was perfused into the vein graft under a distending pressure of 20 mmHg for 10 minutes at room temperature before arteriovenous anastomosis. [score:1]
We continued to assess whether miR-126-3p had the ability to increase HSVEC migration. [score:1]
Effect of miR-126-3p on the proliferation and migration of HSVECs. [score:1]
Exogenous miR-126-3p improved blood flow in vein grafts in vivo. [score:1]
Consistent with the findings for the vascular diameter, the peak-systolic velocity was significantly lower in the miR-126-3p agomir -treated group than in the NC agomir group and vein graft group (130 ± 9.31 cm/s vs. [score:1]
This result is in agreement with the results of earlier studies that the endothelial cell-enriched and vasculoprotective miR-126-3p level was significantly lower in patients with stable CAD [38]. [score:1]
Moreover, hematoxylin eosin staining revealed that treatment with the miR-126-3p agomir dramatically reduced neointimal thickness, supporting earlier observations in balloon-injured arteries in rats and rabbits [27, 28]. [score:1]
To the best of our knowledge, no studies to date have investigated the role of miR-126-3p associated with vein graft disease. [score:1]
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4
[+] score: 152
Other miRNAs from this paper: rno-mir-126a
To test whether Niaspan treatment regulates miR-126 and therefore regulates target gene VEGF and VCAM-1 expression. [score:7]
A report suggests that endothelial cells express miR-126, which inhibits VCAM-1 expression 17. [score:7]
MiR-126 has many target genes, such as VEGF and VCAM-1. Upregulation of VEGF-responsive miRNA constituted key miRNA signatures, reflecting ongoing pathologic changes of early DR 35. [score:6]
Niaspan ameliorates the decrease of miR-126 and regulates miR-126 target gene expression in Diabetic Retinopathy. [score:6]
Niaspan inhibits leukocyte adhesion and inflammatory may via regulating VCAM-1 expression by miR-126. [score:6]
In this study, by a common animal mo del of STZ -induced DR, we show that STZ injection induced diabetes significantly induces DR, while long term of Niaspan treatment diabetes rats slowed down the formation and development of DR, by increasing serum HDL and retinal miR-126 expression as well as increasing Ang1/Tie2 expression. [score:6]
Niaspan treatment of Diabetic Retinopathy decreases miR-126 target gene VEGF/VEGFR and VCAM-1 expression in the retina. [score:5]
Pretreatment with miR-126 -inhibitors bring down the reduction of VEGF and the increase of Ang-1 expression which resulted in by Niaspan in hyperglycemia -induced HREC cells (P < 0.05, Fig. 6B,C). [score:5]
Moreover Niaspan treatment of DR also decreases miR-126 target gene VEGF/VEGFR and VCAM-1/CD45 expressions in retina of DR rats. [score:5]
Meantime, inhibition of miR-126 weakens the increase of Ang-1 expression induced by Niaspan in the HREC. [score:5]
HREC cells were treated miR-126 inhibitor (miR-126 -inhibitor) (Invitrogen, CA, USA) using Lipofectamine 2000. [score:5]
Diabetes also decreases circulating endothelial progenitor cells (EPC) miR-126 expression and impair EPC function via its target, Spred-1 and VEGF 33. [score:5]
Niaspan treatment of Diabetic Retinopathy increases miR-126 target gene Ang-1/Tie-2 expression in the retina. [score:5]
We examined the effect of miR-126 on VEGF and Ang-1 expressions in HREC pretreated with miR-126 -inhibitors by immunoblotting. [score:5]
As shown in the Fig. 6: hyperglycemia significantly decreases miR-126 expression in the hyperglycemia -induced cells and miR-126 -inhibitor pretreatment cells compared to the normal control cells (P < 0.05). [score:4]
Previous studies also shown that miR-126 regulates Ang-1 signaling and vessel maturation by targeting p85 β 40. [score:4]
MiR-126 may halt the hypoxia-induce neovascularization by suspending the cell cycle progression and inhibiting the expression of VEGF 32. [score:4]
Hence, Niaspan regulates Ang1/Tie2 expression may get through miR-126 pathway. [score:4]
However, Niaspan -treated DR significantly increased the expression of microRNA-126 which has been proven is a key positive regulator of angiogenic signaling in endothelial cells and of vascular integrity 18. [score:4]
In conclusion, our data suggests that the Niaspan treatment of DR increases of retina miR-126, Ang-1/Tie-2 level, decreases VEGF/VEGFR and VCAM-1 expressions, which may contribute to the stabilization and maturation of growing blood vessels, decrease BRB damage and neovascularization thus slow down the progression of DR. [score:3]
Expression of miR-126 in the retina of diabetic retinopathy. [score:3]
So, Niaspan could suppress the high levels of VEGF and finally overcome the diabetic -induced retinal neovascularization by increasing miR-126. [score:3]
However, the Niaspan treatment significantly enhance the level of retinal miR-126 expression (P < 0.05, Fig. 3). [score:3]
The expression of miR-126 was reduced in the retina tissue of streptozotocin -induced diabetic rats 32. [score:3]
Here we show that Niaspan-treatment significantly increases retina miR-126, but decreases retina VEGF/VEGFR2 expression. [score:3]
Moreover, in vitro experiment suggests that the inhibition of miR-126 may influence the effects of Niaspan on VEGF. [score:3]
Circulating miR-126 expression was significantly decreased in type 1 diabetes patients than that of the healthy controls 31. [score:3]
Real time PCR was performed for miR-126 expression. [score:3]
Niaspan treatment increase retina miR-126 expression. [score:3]
However, Niaspan intervention markedly increases the miR-126 expression in the HREC (P < 0.05, Fig. 6A). [score:3]
Quantitative real-time reverse transcription PCR assay for microRNA-126 (miR-126) expression. [score:2]
The miR-126 may play an important role in the regulation of DR procedure. [score:2]
MiR-126 has several target genes such as VEGF and VCAM-1 17 18. [score:2]
Consistent with previous studies, we found that DR significantly decreases retina miR-126 expression compared to normal control rats. [score:2]
We performed quantitative real-time reverse transcription-PCR assay for miR-126 expression in retina and HREC. [score:2]
Decreasing miR-126 level induces endothelial injury and participate in the development and progression of diabetic vascular complications 34. [score:2]
MiR-126, the miRNA considered to be specially expressed in endothelial cells, is strongly associated with angiogenesis. [score:2]
, USA) (NA group); 25 mM D-glucose (hyperglycemia) + Niacin (1 mM) + microRNA126 inhibitor (NI group). [score:2]
The reduction of miR-126 levels was detected in the retina of diabetic rats. [score:1]
Role of miR-126 in diabetic retinopathy. [score:1]
In this study, we found that Niaspan treatment of DR significantly increases miR-126 and Ang1/Tie2 signaling activity in the retina. [score:1]
To understand the mechanisms of Niaspan treatment induced protective effect in DR rats, miR-126 expression was measured. [score:1]
All the procedure have shown in the picture Fig. 7. Further investigation of mechanism of miR-126 would be important in developing new therapeutic targets for preventing and reversing diabetic retinopathy. [score:1]
[1 to 20 of 43 sentences]
5
[+] score: 133
Other miRNAs from this paper: rno-mir-126a
Obesity downregulates the expression of miR-126, which consequently prevents the expression of several angiogenic proteins. [score:8]
Phosphatidylinositol 3-kinase regulatory subunit beta (PI3KR2) is one of the main targets of miR-126 and controls the vascular endothelial growth factor (VEGF) signaling pathway via direct inhibition of phosphatidylinositol 3-kinase (PI3K α-110). [score:7]
We show here that obesity decreased miR-126 expression, which increased the protein content of its target genes. [score:5]
Other studies have shown that ET restores the expression of miR-126 in other diseases [17]. [score:5]
The miR-126 contributes to vascular homeostasis in mature endothelial cells, associated with maintaining vascular integrity and inhibiting proliferation and motility, in this case actins as an angiogenesis suppressor. [score:5]
However, in other chronic diseases, such as diabetes mellitus II, it has previously been demonstrated that there is also a decrease in the expression of miR-126 in the circulation of rats and humans. [score:5]
However, training restored the expression of miR-126 and consequently normalized PI3KR2 expression in obese rats. [score:5]
In conclusion, miR-126 plays an important role in the control of angiogenic pathways by targeting the expression of PI3KR2. [score:5]
The expression of miR-126 increases in healthy trained rats [19] and is severely decreased in rats with chronic diseases such as hypertension [17]. [score:5]
The results of this study indicate that miR-126 is downregulated in the skeletal muscle of obese rats and this change was associated with capillary rarefaction. [score:4]
PI3KR2 is one of the validated targets of miR-126 and is an important factor in the regulation of angiogenesis. [score:4]
Thus, miR-126 inhibits PI3KR2 and promotes angiogenesis through an indirect increase in PI3K and VEGF. [score:4]
Knockdown of miR-126 expression in animals results in an impairment in the formation and maintenance of blood vessels and partial embryonic lethality [7]. [score:4]
However, aerobic exercise training is able to normalize the expression of miR-126 and consequently restore the function of various proteins controlled by it. [score:3]
Furthermore, ET was also effective in increasing the expression of miR-126 in the LTR group (LS: 100 ± 13.1; LTR: 140 ± 10.7; OB: 55 ± 6.8; and OBTR: 92 ± 6.4). [score:3]
Indeed, our data show that there is a correlation between miR-126 expression and the capillary/fiber ratio. [score:3]
Our study shows, for the first time, that ET restores miR-126 expression in the skeletal muscle of obese Zucker rats and is involved in exercise -induced angiogenesis. [score:3]
The possible molecular factors that precede this impaired phenotype in obesity may include the expression of miR-126 and proteins of the VEGF pathway. [score:3]
In the present study, we found that reduced miR-126 levels induced capillary rarefaction in skeletal muscle by targeting PI3KR2 in obese Zucker rats. [score:3]
In this study, an increase in the expression of miR-126 was accompanied by increased capillarity (Figure 4(b)). [score:3]
In contrast, ET restored miR-126 expression in the OBTR group toward control levels. [score:3]
Decreased miR-126 led to increases PI3KR2 protein expression in obese rats. [score:3]
PI3KR2 is a target gene of miR-126. [score:3]
Our previous studies have shown that, in healthy rats, ET increases cardiac miR-126 expression, promoting cardiac angiogenesis [19]. [score:3]
However, in cases of vascular lesion, hypoxia or stress on the vessel wall, there is an increase in the expression of miR-126, which activates endothelial cells and endothelial progenitor cells, which contributes to vascular healing and the formation of new vessels [22]. [score:3]
We were the first to show that sedentary obese animals present a decrease in miR-126 expression, which contributes to microvascular rarefaction. [score:3]
Moreover, we also showed that ET normalizes the expression of miR-126 and reverses the capillary loss caused by obesity (Figure 6). [score:3]
miR-126 is an endothelial specific miR (angiomiR) and its expression is closely linked to angiogenesis. [score:3]
ET counteracted this effect by restoring the expression of miR-126 and skeletal muscle capillarity in obese Zucker rats. [score:3]
Effect of Exercise Training and Obesity on miRNA-126 Expression and Relation with Angiogenesis. [score:3]
The literature demonstrates that only a prolonged ET session in humans leads to increased expression of miR-126 in the circulation [25]. [score:3]
Expression of miR126 is enriched in endothelial cells and endothelial progenitor cells. [score:3]
Our data show that miR-126 expression was reduced in the OB group compared with all the other groups. [score:2]
Knockdown of miR-126 in animals leads to impaired vascular formation due to a reduction in the migration of endothelial cells during the genesis of vessels; this compromises blood vessel integrity and leads to hemorrhage in the embryonic period [18]. [score:2]
Our evidence suggests that miR-126 also influences control of the microvasculature in the skeletal muscle of obese Zucker rats. [score:1]
However, ET has been shown to restore miR-126 levels in the skeletal muscle of hypertensive rats and induces angiogenesis [17]. [score:1]
Moreover, there is a correlation between the decrease of mir-126 and endothelial apoptosis. [score:1]
MiR-126 controls angiogenesis and regulates the formation, survival, and maintenance of new vessels [16– 18]. [score:1]
It is important to note that a time course study in a type 2 diabetic rat mo del shows that the gradual decrease of miR-126 and other angiomiRs precedes endothelial apoptosis and decreased vascular integrity, as well as changes in the density of the microvasculature [23]. [score:1]
Analysis of miR-126. [score:1]
[1 to 20 of 40 sentences]
6
[+] score: 76
Other miRNAs from this paper: rno-mir-126a, rno-mir-210, rno-mir-1
14, 15 In fact, miR-126 activates survival kinases including ERK and Akt by downregulation of its targets and enhances the actions of VEGF. [score:6]
MiR-126 is a pro-angiogenic miR, which is strongly expressed in the heart endothelium and directly targets SPRED1 and PIK3R2 for repression and functions to promote VEGF signaling. [score:6]
MiRNA-126 is strongly expressed in the heart endothelium and targets Sprouty-related protein-1 (Spred-1), PIK3R2, a regulatory subunit of PI3K. [score:5]
For the first time, our study demonstrated that heart miR-126 and its related pathways including Akt and ERK1/2 upregulated in response to crocin combined with voluntary exercise in rats. [score:4]
Two-way ANOVA showed that the miR-126 expression were significantly higher in rats treated with crocin (p < 0.001), voluntary exercise (p < 0.01) and crocin combination with exercise (p < 0.001) than in control rats. [score:3]
Figure 4Effect of crocin and voluntary exercise on miR-126 expression levels. [score:3]
In the present study, we demonstrated that miR-126 and miR-210 expression of rat cardiac tissue increased in crocin, voluntary exercise, and exercise-crocin groups. [score:3]
This study shows that crocin in combination with voluntary exercise promotes cardiac angiogenesis and this may be related to expression of miRNA-126 and miR-210. [score:3]
In addition, we showed that ERK1/2 and Akt levels increased under high expression of miR-126. [score:3]
[24] Expression of miR-126 and miR-210 was assessed by qRT-PCR. [score:3]
Therefore, it seems that voluntary exercise relieves the repressive influence of Spred-1/PI3K on the Akt and ERK1/2 by miR-126 overexpression, which finally improves cardiac angiogenesis. [score:3]
Effects of crocin combined with voluntary exercise on miR-126 expression in the heart tissue. [score:3]
In addition, we showed that crocin combination with voluntary exercise has synergistic effects on miR-126 expression and Akt, ERK1/2 levels in heart tissue, which was the first study in rat cardiac angiogenesis. [score:3]
In addition, combination of exercise and crocin amplified their effect on miR-126 and miR-210 expression, and angiogenesis. [score:3]
In line with our results, Uhlemann et al. [33] reported that miR-126 expression increased after acute endurance exercise. [score:3]
The present study was undertaken to clarify the effect of crocin and voluntary exercise on miR-126 and miR-210 expression in cardiac myocytes of diabetic rats. [score:3]
Crocin and voluntary exercise improve heart angiogenesis possibly through enhancement of miR-126 and miR-210 expression. [score:3]
MiR-126, miR-210 expression and CD31 in the heart increased in both crocin and voluntary exercise groups compared with control group. [score:2]
[18] In the present study, we showed that miR-126 regulates heart angiogenesis via Akt and ERK1/2 pathways in response to crocin and voluntary exercise. [score:2]
In the rats that underwent voluntary exercise and simultaneously received crocin for 8 weeks, expression of heart miR-126 significantly increased compared with Exe (p < 0.01), and Cro (p < 0.001) groups (Figure 4). [score:2]
[36] In this study, we also showed that crocin regulates heart angiogenesis through miR-126 and its related Akt and ERK1/2 pathways. [score:2]
The 2 [-(ΔΔCt)] method was used to determine relative quantitative levels of miR-126 and miR-210. [score:1]
The aim of this study was to evaluate the effect of crocin and voluntary exercise on miR-126 and miR-210 expression levels and angiogenesis in the heart tissue. [score:1]
Akt, ERK1/2 protein levels, miR-126 and miR-210 expression were measured in the heart tissue. [score:1]
For Akt, ERK, CD31, miR-126, and miR-210 parameters, data were analyzed using two-way ANOVA followed by Tukey's post hoc test. [score:1]
Therefore, we suggest that crocin by increasing of miR-126 and enhancement of VEGF signaling pathways through Akt and ERK1/2 can induce cardiac capillary formation. [score:1]
Major findings also emerge from Fernandes et al. [34] study indicating that exercise training restored the levels of peripheral miR-126 associated with revascularization in hypertension. [score:1]
[40] Based on the present results it could be concluded that crocin pretreatment improved cardiac angiogenesis, the effect which can be attributed to its ability of increasing Akt and ERK1/2 levels via enhancement of miR-126. [score:1]
11- 13 MiR-126 is one of the few miRNAs that is an endothelial cell-specific miRNA and plays an essential role in neoangiogenesis. [score:1]
[1 to 20 of 29 sentences]
7
[+] score: 39
miR-99a and miR-30b were confirmed to be the up-regulated miRNAs in ARDS, while miR-126 and miR-26a were confirmed to be down-regulated miRNAs in ARDS (Figure  2). [score:7]
The down-regulated miRNAs included miR-24, miR-26a, miR-126, and Let-7a, b, c, f. The up-regulated miRNAs were composed of miR-344, miR-346, miR-99a, miR-127, miR-128b, miR-135b, and miR-30a/b. [score:7]
miR-126, a regulator of angiogenic signaling and vascular integrity, has been reported to be involved in ARDS/ALI and VEGF is identified as a target of miR-126 [13, 14]. [score:4]
In the present study, we found that miR-126 was down-regulated in ARDS. [score:4]
The down-regulated miRNAs included miR-24, miR-26a, miR-126, and Let-7 family members. [score:4]
miR-126 controls TLR2/4 inflammatory signaling pathways by modulating TOM1 expression in cystic fibrosis lung [45]. [score:3]
VEGF is a well-defined ARDS -associated candidate gene, and is a target of miR-126 [13, 14]. [score:3]
miR-126 controls leukocyte infiltration into inflamed lungs by repressing ALCAM expression [52]. [score:3]
In addition, miR-126 is down-regulated in cystic fibrosis that is characterized by chronic airway inflammation. [score:2]
Moreover, miR-126 also plays a role in neoangiogenesis of adult tissues in response to injury [38]. [score:1]
However, we did not find the correlation of miR-126 to the identified altered mRNAs in ARDS. [score:1]
[1 to 20 of 11 sentences]
8
[+] score: 34
These data suggest that down-regulation of let7c, miR29a and miR29c, and miR126 may be a major event during cataract formation in the SCR, as changes in miRNA expression levels were increased in cataractous lenses. [score:6]
Of the latter, miR126, miR136, miR206, miR451 and miR551b showed significant, gradual down-regulation (>2 times) after birth or during development (ED16>4W>4W). [score:5]
Relative expression of miRNAs let7b, let7c, miR-29a, miR29c and miR126, which are significantly up- or down-regulated during the progression of lens development, were measured following RNA extraction using RT-PCR. [score:5]
In contrast, miR126 and miR-451 were significantly down-regulated (Fig. 2). [score:4]
Interestingly, RT-PCR assessment of level of miRNAs in cataractous lenses showed that four miRNAs–let7c, miR29a and 29c, and miR-126–were significantly down-regulated, suggesting a plausible contribution by these miRNAs to cataractogenesis (Fig. 3). [score:4]
Relative expression levels of miRNAs, let-7b, let-7c, miR-29a, miR-29c, miR-204, miR-126, miR-451 in ED16, 4W and 14W lenses are represented as histograms with normalized averages ± SD. [score:3]
However, expression of these miRNAs and miR126 was decreased in SCRs with cataract. [score:3]
However, let7c, miR-29a, miR29c and miR126 were significantly down-regulated in SCR with cataract lenses compared with SCR without cataract lenses at both ages 7 and 21 weeks. [score:3]
The seven miRNAs (let7b, 7c, miR29a, miR-29c, miR204, miR126, miR51) listed in Table 3 were used for validation experiments. [score:1]
[1 to 20 of 9 sentences]
9
[+] score: 33
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]
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]
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]
For example, miRNAs involved in cardiac hypertrophy and heart failure such as miR-208, miR-133, miR-195, miR-21, and miR-126 have been reported in several studies [5- 8]. [score:1]
[1 to 20 of 6 sentences]
10
[+] score: 30
Other miRNAs from this paper: rno-mir-126a, rno-mir-191a, rno-mir-191b
Previous study showed that asthmatic inflammation was associated with upregulation of miRNA-126 (Kabesch et al., 2012). [score:4]
sensitized group: **; p< 0.01 Figure 2Real-time quantitative RT-PCR analysis of miR-126 expression level in lung of control (C), sensitized (S), S pretreated with thymoquinone (S+TQ), S pretreated with alpha-hederin (S+AH) rats (for each group, n = 6). [score:3]
It may intervene in miRNA-126 expression, which consequently could interfere with IL-13 secretion pathway leading to a reduction in inflammatory responses. [score:3]
Alpha-hederin may intervene in miRNA-126 expression, which could consequently interfere with IL-13 secretion pathway leading to a reduction in inflammatory responses. [score:3]
The expression profile of miR-126 was performed on total RNA extracts by the aid of universal cDNA synthesis kit according to instruction manual of Exiqon. [score:3]
As IL-13 is central to the progression of asthma and many miRNAs such as miRNA-126 can regulate its production directly and indirectly (Greenet al., 2013 ▶), in this study we have evaluated the preventive effect of alpha -Hederin on lung pathology, IL-13 mRNA and miRNA-126 in ovalbumin-sensitized male rats in order to elicit its mechanism. [score:2]
MiRNA-126 gene expression was increased significantly in all sensitized groups in comparison to C group (p<0.001 to p<0.01). [score:2]
Alpha-hederin MiRNA-126 IL-13 mRNA Ovalbumin Thymoquinone Asthma Asthma is an airways chronic inflammatory disease which has recently become epidemic in developed countries (Mattes et al., 2009 ▶). [score:2]
Lung miRNA-126 was significantly increased during sensitization protocol of this study. [score:1]
Although alpha-hederin decreased the levels of miRNA-126, IL-13 mRNA and pathological changes in comparison with thymoquinone, the results were statistically not significant. [score:1]
Therefore, it was suggested that alpha-hederin and thymoquinone with used concentrations in current study might decrease miRNA-126 and consequently attenuate the IL-13 secretion pathway leading to decreased inflammatory pathological changes in lung tissue. [score:1]
The level of miRNA-126 was very high in patients with asthma following Th2 activity. [score:1]
Thymoquinone and alpha-hederin in administered dose resulted in the decline of miRNA-126 expression in lungs of sensitized pretreated groups in this investigation. [score:1]
Housekeeping beta-glucuronidase gene was used to normalize the amount of PCR products for mRNA samples, and rno-miR-191 for miRNA-126. [score:1]
The 2 [-(Ct)] method was utilized in order to determine relative-quantitative levels of individual mRNAs and miR-126. [score:1]
Levels of IL-13 mRNA and miRNA-126 in lung tissue and its pathological changes in each group were assessed. [score:1]
[1 to 20 of 16 sentences]
11
[+] score: 28
With exception of miRNA-155, down-regulated in serum of AMD patients and in serum of Aβ injected rats, six miRNAs (miR-9, miR-23a, miR-27a, miR-34a, miR-146a, miR-126) showed an up-regulation in serum of AMD patients. [score:7]
Analysis of these 13 miRNAs revealed that 7 miRNAs showed a significant up-regulation in serum of AMD patients in comparison to control group (miR-9, miR-23a, miR-27a, miR-34a, miR-146a, miR-155, and miR-126). [score:4]
In particular, up-regulation of miR-9, miR-23a, miR-27a, miR-34a, miR-126, and miR-146a was found in serum of AMD patients. [score:4]
MicroRNA-126 inhibits ischemia -induced retinal neovascularization via regulating angiogenic growth factors. [score:3]
The following groups of miRNAs were analyzed: miR-27a, miR-146a, miR-155 miR-9, miR-23a, miR-27a, miR-34a, miR-126,miR-146a, miR-155 miR-155 GraphPad Prism (version 4.0; GraphPad Software, San Diego, CA, USA) was used for statistical analysis and graphical representation of miRNA differential expression data. [score:3]
In conclusion, the modified miRNA levels we found in rat retina (miR-27a, miR-146a, miR-155) and serum of AMD patients (miR-9, miR-23a, miR-34a, miR-126, miR-27a, miR-146a, miR-155) suggest that, among others, miR-27a, miR-146a, and miR-155 have an important role in AMD and could represent suitable biomarkers and appealing pharmacological targets. [score:3]
Incidentally, we showed that changes in circulating levels of some miRNAs (miR-9, miR-23a, miR-27a, miR-34a, miR-126, miR-146a, miR-155) as found in AMD patients are associated to Alzheimer's disease and modulate genes involved in neurodegenerative and inflammatory pathways. [score:3]
Converging miRNA functions in diverse brain disorders: a case for miR-124 and miR-126. [score:1]
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12
[+] score: 28
Two differences that occurred in the current study were downregulation of miR-126 and miR-145 in MCT PAH rats, which had previously been reported as upregulated in human iPAH specimens and BMPR2 deficient mice [12]. [score:7]
MiR-17 was upregulated in the paraffin sections, but not in the fresh specimens, whereas miR-126, 145, 150 and 328 were not significantly downregulated in the paraffin sections as compared to the fresh specimens. [score:6]
MiR-126 expression was decreased in PLs and CLs from PAH subjects relative to unremo deled control PA, but miR-126 expression was nevertheless significantly higher in PLs than in CLs of PAH specimens. [score:5]
A group of miRNAs were downregulated in the lung and PA of MCT PAH rats, including miR-126, miR-145, miR-150, miR-424, and miR-503 (Fig 1A and 1B). [score:4]
MiR-126 expression was also decreased in laser microdissected concentric and plexigenic lesions of human PAH specimens compared to expression in unremo deled human control specimens in the Bockmeyer study, consistent with our findings in MCT PAH. [score:3]
Expression levels of miR-17-5p, miR-21-5p, miR-126-3p, miR-145-5p, miR-150-5p, miR-204-5p, miR-223-3p, miR-328-3p, miR-424-5p (mmu-miR-322, the mouse/rat ortholog for hsa-miR-424), and miR-503-5p were evaluated. [score:1]
N = 4. p values are as follows: MiR-126 p = 0.499, miR-145 p = 0.422, miR-150 p = 0.803. [score:1]
As shown in Fig 2, the levels of miR-126, 145 and 150 were similar when normalized to either a C. elegans miR39 standard or an internal miR-103 control (Fig 2). [score:1]
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13
[+] score: 26
For that reason, rather than selecting the common targets to both algorithms, we chose PicTar algorithm to match upregulated miRNAs (miR-21, miR-98, miR-27a, miR-143, let-7d, miR-126, miR-22) with downregulated putative targets in Ortis et al. and vice versa (Table 4). [score:11]
Eight miRNAs from the PCR-confirmed 11 miRNAs, are common to both in vitro and in vivo inflammation conditions; 7 upregulated (miR-21, miR-98, miR-27a, miR-143, let-7d, miR-126 and miR-22) and one (miR-129) downregulated (Table 3). [score:7]
Using quantitative PCR -based high throughput analysis, we have confirmed upregulation of 7 (miR-21, miR-98, miR-27a, miR-143, let-7d, miR-126, and miR-22) and downregulation of 1 (miR-129) miRNAs out of the 26 activated miRNAs identified in our settings. [score:7]
Low plasma levels of miR-21 and miR-126 have been detected in patients with type 2 diabetes [92]. [score:1]
[1 to 20 of 4 sentences]
14
[+] score: 19
Interestingly, the LII up-regulated miR-26b and miR-126 are implicated in Alzheimer’s disease (Absalon et al. 2013; Kim et al. 2014), while the LDeep up-regulated miR-219 and miR-7a/b are implicated in schizophrenia (Beveridge and Cairns 2012), diseases which both show pathologies in LII. [score:11]
The two miRNAs with the lowest p value up-regulated in LII (miR-143 and miR-126; Fig.   1f) are involved in angiogenesis (Climent et al. 2015; Sonntag et al. 2012). [score:4]
Several of the differentially expressed miRNAs regulate neuron differentiation, including miR-126 and miR-26b in LII, and miR-7a/b in LDeep. [score:4]
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15
[+] score: 17
The majority of these progression -associated miRNAs, including miR-10a, miR10b, miR-124, miR-125b, miR-126, miR-145, were increasingly downregulated with increasing lesion severity, while 2 miRNAs, miR-21 and miR-200a, were upregulated with advancing tumor progression. [score:7]
Several of the progression -associated miRNAs identified mirror those found to be changed during progression in human normal, DCIS, and IDC breast cancer samples, including an upregulation of miR-21 and a downregulation of miR-10b, miR-125b, and miR-126 [15]. [score:7]
The 8 miRNAs we found from our profiling (specifically, miR-10a, miR-10b, miR-21, miR-124, miR-125b, miR-126, miR-145, and miR-200a) each showed progressive changes in expression with advancing lesion grade. [score:3]
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16
[+] score: 14
In 2008, Wu et al. first reported 11 differentially expressed miRNAs in colon tissues that were closely associated with UC patients in the active period, of which miR-126 expression was upregulated [33]. [score:8]
miR-126 participated in immune inflammation and carcinogenesis processes in the colon [33, 37, 38] and could directly bind to the 3′-UTR region of the target gene I κB to regulate the NF- κB signaling pathway [39]. [score:5]
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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17
[+] score: 13
In response to 4 hours of mechanical stretch, rno-miR-322, let-7f, miR-103, miR-126, miR-494, miR-126*, miR-130b and miR-195 were significantly dysregulated (Fig.   7A and Supplementary Dataset  5), so we sought potential mRNA targets for these dysregulated miRNAs among the stretch-regulated genes in 4 and 12 hours timepoints. [score:6]
At a later time point i. e. 12 hours of mechanical stretching, only rno-miR-126 exhibited any significantly (P < 0.05) dysregulated expression in response to unstretched cells. [score:4]
In response to 1 hour of mechanical stretching, only one miRNA, rno-miR-130b showed differential expression compared to controls (P < 0.05), whereas 8 miRNAs (rno-miR-322, rno-let-7f, rno-miR-103, rno-miR-126, rno-miR-494, rno-miR-126*, rno-miR-130b, rno-miR-195; P < 0.05) were dysregulated in response to 4 hours of stretch (Supplemental Dataset  5). [score:3]
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18
[+] 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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19
[+] score: 10
Although miR-155 and miR-126 have been demonstrated to promote intestinal inflammation in IBD by inhibiting the expression of NF- κB inhibitor I κB α [59, 60], they are not the miRNA targets in HPM treatment on Tianshu and Qihai of experimental CD rats, indicating that HPM has specificity in terms of gene regulation. [score:10]
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20
[+] score: 9
Other miRNAs from this paper: rno-mir-126a, rno-mir-222, rno-let-7g
In addition, miRNA expression analysis (Fig.   4e) evidenced an increased expression of miR-126-5p, an endothelial cell-specific regulator of angiogenesis and vascular integrity 29, 30. [score:6]
For analysis of miRNA expression, the following commercial kits were used: mirVana miRNA isolation Kit (Invitrogen), TaqMan Advanced miRNA cDNA Synthesis Kit (Applied Biosystems) and the TaqMan Advanced miRNA Assays: rno-miR-126-3p, rno-miR-126-5p, rno-miR-222-3p and rno-let-7g-5p. [score:2]
Wang S The endothelial-specific microRNA miR-126 governs vascular integrity and angiogenesisDev. [score:1]
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21
[+] score: 9
Recently, a programmed increase in miR-126, was shown to repress translation of its Irs1 target in WAT from mice exposed to maternal overnutrition in early life [8]. [score:5]
However, none of the candidate miRNAs (including miR-126) were upregulated in adipocytes that were differentiated in utero in response to maternal low protein diet. [score:4]
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[+] score: 9
Zernecke et al. [30] showed that miR-126 targeted vascular smooth muscle cells in atherosclerotic rat mo dels. [score:3]
Additionally when the patients were grouped based on the TOAST classification, as large artery (LA), cardioembolic (CE) and small vessel (SV), 57 miRNAs (let-7a, let-7d*, let-7g, let-7i, miR-126, -1261, -1299, -130a, -1321, -135b, -184, -187*, -18a*, -208a, -214, -20a, -22*, -26b, -26b*, -27a*, -30b, -30c, -30e*, -320b, -320d, -324-5p, -331-3p, -340, -342-3p,-361-5p, -363, -370, -381, -422a, -423-3p, -494, -501-5p, -502-3p, -505*, -525-5p, -549, -552, -553, -574-3p, -574-5p, -585, -602, -611, -617, -627, -629, -675, -7, -886-5p, -92a, -93* and -96) were identified to be significantly dysregulated among them. [score:2]
Though miR-920 has not been found in normal developing human brain [17], it may function similarly to miR-126 in atherosclerosis [30]. [score:1]
Zampetaki A. Kiechl S. Drozdov I. Willeit P. Mayr U. Prokopi M. Mayr A. Weger S. Oberhollenzer F. Bonora E. MicroRNA profiling reveals loss of endothelial miR-126 and other microRNAs in type 2 diabetesCirc. [score:1]
Zernecke A. Bidzhekov K. Noels H. Shagdarsuren E. Gan L. Denecke B. Hristov M. Köppel T. Jahantigh M. N. Lutgens E. Delivery of microRNA-126 by apoptotic bodies induces CXCL12 -dependent vascular protectionSci. [score:1]
Setting cycle threshold values (C [T]) of 32 as a cut-off, a final panel of 32 miRNAs (let-7a, let-7d*, let-7g, let-7i, miR-126, -130a, -187*, -18a*, -20a, -22*, -26b, -30b, -30c, -30e*, -320b, -320d, -324-5p, -331-3p, -340, -342-3p, -361-5p, -363, -422a, -423-3p, -501-5p, -502-3p, -505*, -574-3p, -675, -886-5p, -92a and -93*) that could significantly distinguish the stroke etiology was obtained. [score:1]
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23
[+] score: 9
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-16-1, hsa-mir-17, hsa-mir-18a, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-20a, hsa-mir-22, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-98, hsa-mir-101-1, hsa-mir-16-2, mmu-let-7g, mmu-let-7i, mmu-mir-1a-1, mmu-mir-15b, mmu-mir-101a, mmu-mir-126a, mmu-mir-130a, mmu-mir-133a-1, mmu-mir-142a, mmu-mir-181a-2, mmu-mir-194-1, hsa-mir-208a, hsa-mir-30c-2, mmu-mir-122, mmu-mir-143, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-181a-1, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-15b, hsa-mir-122, hsa-mir-130a, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-142, hsa-mir-143, hsa-mir-126, hsa-mir-194-1, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-208a, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-15a, mmu-mir-16-1, mmu-mir-16-2, mmu-mir-18a, mmu-mir-20a, mmu-mir-22, mmu-mir-26a-1, mmu-mir-26b, mmu-mir-29c, mmu-mir-98, mmu-mir-326, rno-mir-326, rno-let-7d, rno-mir-20a, rno-mir-101b, mmu-mir-101b, hsa-mir-1-1, mmu-mir-1a-2, hsa-mir-181b-2, mmu-mir-17, mmu-mir-19a, mmu-mir-181a-1, mmu-mir-26a-2, mmu-mir-19b-1, mmu-mir-181b-1, mmu-mir-181c, hsa-mir-194-2, mmu-mir-194-2, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-101-2, hsa-mir-26a-2, hsa-mir-378a, mmu-mir-378a, hsa-mir-326, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, mmu-mir-181b-2, rno-let-7a-1, rno-let-7a-2, rno-let-7b, rno-let-7c-1, rno-let-7c-2, rno-let-7e, rno-let-7f-1, rno-let-7f-2, rno-let-7i, rno-mir-15b, rno-mir-16, rno-mir-17-1, rno-mir-18a, rno-mir-19b-1, rno-mir-19a, rno-mir-22, rno-mir-26a, rno-mir-26b, rno-mir-29c-1, rno-mir-30c-1, rno-mir-30c-2, rno-mir-98, rno-mir-101a, rno-mir-122, rno-mir-126a, rno-mir-130a, rno-mir-133a, rno-mir-142, rno-mir-143, rno-mir-181c, rno-mir-181a-2, rno-mir-181b-1, rno-mir-181b-2, rno-mir-194-1, rno-mir-194-2, rno-mir-208a, rno-mir-181a-1, hsa-mir-423, hsa-mir-18b, hsa-mir-20b, hsa-mir-451a, mmu-mir-451a, rno-mir-451, ssc-mir-122, ssc-mir-15b, ssc-mir-181b-2, ssc-mir-19a, ssc-mir-20a, ssc-mir-26a, ssc-mir-326, ssc-mir-181c, ssc-let-7c, ssc-let-7f-1, ssc-let-7i, ssc-mir-18a, ssc-mir-29c, ssc-mir-30c-2, hsa-mir-484, hsa-mir-181d, hsa-mir-499a, rno-mir-1, rno-mir-133b, mmu-mir-484, mmu-mir-20b, rno-mir-20b, rno-mir-378a, rno-mir-499, hsa-mir-378d-2, mmu-mir-423, mmu-mir-499, mmu-mir-181d, mmu-mir-18b, mmu-mir-208b, hsa-mir-208b, rno-mir-17-2, rno-mir-181d, rno-mir-423, rno-mir-484, mmu-mir-1b, ssc-mir-15a, ssc-mir-16-2, ssc-mir-16-1, ssc-mir-17, ssc-mir-130a, ssc-mir-101-1, ssc-mir-101-2, ssc-mir-133a-1, ssc-mir-1, ssc-mir-181a-1, ssc-let-7a-1, ssc-let-7e, ssc-let-7g, ssc-mir-378-1, ssc-mir-133b, ssc-mir-499, ssc-mir-143, ssc-mir-423, ssc-mir-181a-2, ssc-mir-181b-1, ssc-mir-181d, ssc-mir-98, ssc-mir-208b, ssc-mir-142, ssc-mir-19b-1, hsa-mir-378b, ssc-mir-22, rno-mir-208b, rno-mir-133c, hsa-mir-378c, ssc-mir-194b, ssc-mir-133a-2, ssc-mir-484, ssc-mir-30c-1, ssc-mir-126, ssc-mir-378-2, ssc-mir-451, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, mmu-mir-378b, mmu-mir-101c, hsa-mir-451b, hsa-mir-499b, ssc-let-7a-2, ssc-mir-18b, hsa-mir-378j, rno-mir-378b, mmu-mir-133c, mmu-let-7j, mmu-mir-378c, mmu-mir-378d, mmu-mir-451b, ssc-let-7d, ssc-let-7f-2, ssc-mir-20b-1, ssc-mir-20b-2, ssc-mir-194a, mmu-let-7k, mmu-mir-126b, mmu-mir-142b, rno-let-7g, rno-mir-15a, ssc-mir-378b, rno-mir-29c-2, rno-mir-1b, ssc-mir-26b
The observation that miR-22, miR-26b, miR-126, miR-29c and miR-30c are ubiquitously expressed in 14 different tissues of pig is interesting. [score:3]
Additionally, many other miRNAs, such as let-7, miR-98, miR-16, miR22, miR-26b, miR-29c, miR-30c and miR126, were also expressed abundantly in thymus (Figure 3). [score:3]
miR-22, miR-26b, miR-29c, miR-30c and miR-126 exhibited almost similar expression patterns in all tissues examined (Figure 3B). [score:3]
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24
[+] score: 7
Furthermore, 40 of the miRNAs, including miR-34b-3p, miR-25-3p, miR-126-5p, miR-142-5p, and miR-324-5p, were only transiently upregulated (Figure  2A); the other 23 miRNAs, including miR-34a-3p and miR-324-5p, were transiently downregulated on the 3rd day but returned to normal levels by the 14th day (Figure  2B). [score:7]
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25
[+] score: 6
Meng Q Wang W Yu X Li W Kong L Qian A Li C Li X Upregulation of MicroRNA-126 contributes to endothelial progenitor cell function in deep vein thrombosis via Its Target PIK3R2J Cell Biochem. [score:5]
In addition, our previous studies showed that miR-150 and miR-126 contributed to EPCs function in vitro and improved thrombus recanalization and resolution in vivo [14, 15]. [score:1]
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[+] score: 6
Additionally, another evidence collected from the current inverstigation demonstrate that the microRNA -mediated regulation is not limited to the 3’UTR, the functionality of target sites in the CDS also confirmed by previous studies [57– 59], such as miR-24 [58], miR-296, miR-470, miR-134 [60], miR-126 [43], miR-181a [59], miR-148 [57] and miR-519 [61] that target sequences within the mRNA coding region have been reported to repress the biosynthesis of the encoded proteins in similar way. [score:6]
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27
[+] score: 6
Other miRNAs from this paper: rno-let-7b, rno-mir-21, rno-mir-30a, rno-mir-126a, rno-mir-155
Paeonol promotes microRNA-126 expression to inhibit monocyte adhesion to ox-LDL-injured vascular endothelial cells and block the activation of the PI3K/Akt/NF-kappaB pathway. [score:5]
Circulating miR-30a, miR-126 and let-7b as biomarker for ischemic stroke in humans. [score:1]
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[+] score: 5
miR-126 regulates angiogenic signaling and vascular integrity. [score:2]
The observed differential regulation of miR-126 suggests that the tissue samples also contained large amounts of vasculature, because expression of this miRNA is well characterized in endothelial cells of zebrafish, mouse and human (Fish et al., 2008; Anand and Cheresh, 2011). [score:2]
To facilitate the analysis of the array data, identical miRNAs of different species (e. g. bta-miR-126 and hsa-miR-126) were grouped together with miRNAs with the same precursor or closely related mature sequences (e. g. mdo-miR-26, hsa-miR-26a), as long as the seed sequences were still conserved. [score:1]
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29
[+] score: 5
Other miRNAs from this paper: rno-mir-126a
Unacylated ghrelin induces oxidative stress resistance in a glucose intolerance and peripheral artery disease mouse mo del by restoring endothelial cell miR-126 expression. [score:5]
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[+] score: 5
Emerging evidence indicates that miRNAs act as key modulators of target gene expression, and some, such as miR-21, miR-126, miR-33, miR-125, and miR-222, have been shown to be involved in the pathogenesis of stroke [5, 6]. [score:5]
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[+] score: 5
We do not observe a similar down-regulation of miR-126 in our samples. [score:4]
The authors discussed the loss of endothelial miR-126 and other miRNAs in T2D. [score:1]
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[+] score: 4
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-17, hsa-mir-18a, hsa-mir-20a, hsa-mir-21, hsa-mir-22, hsa-mir-26a-1, hsa-mir-99a, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-106a, hsa-mir-107, mmu-let-7g, mmu-let-7i, mmu-mir-99a, mmu-mir-101a, mmu-mir-125a, mmu-mir-125b-2, mmu-mir-126a, mmu-mir-127, mmu-mir-145a, mmu-mir-146a, mmu-mir-129-1, mmu-mir-206, hsa-mir-129-1, hsa-mir-148a, mmu-mir-122, mmu-mir-143, hsa-mir-139, hsa-mir-221, hsa-mir-222, hsa-mir-223, mmu-let-7d, mmu-mir-106a, hsa-let-7g, hsa-let-7i, hsa-mir-122, hsa-mir-125b-1, hsa-mir-143, hsa-mir-145, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-127, hsa-mir-129-2, hsa-mir-146a, hsa-mir-206, mmu-mir-148a, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-18a, mmu-mir-20a, mmu-mir-21a, mmu-mir-22, mmu-mir-26a-1, mmu-mir-129-2, mmu-mir-103-1, mmu-mir-103-2, rno-let-7d, rno-mir-335, rno-mir-129-2, rno-mir-20a, mmu-mir-107, mmu-mir-17, mmu-mir-139, mmu-mir-223, mmu-mir-26a-2, mmu-mir-221, mmu-mir-222, mmu-mir-125b-1, hsa-mir-26a-2, hsa-mir-335, mmu-mir-335, rno-let-7a-1, rno-let-7a-2, rno-let-7b, rno-let-7c-1, rno-let-7c-2, rno-let-7e, rno-let-7f-1, rno-let-7f-2, rno-let-7i, rno-mir-17-1, rno-mir-18a, rno-mir-21, rno-mir-22, rno-mir-26a, rno-mir-99a, rno-mir-101a, rno-mir-103-2, rno-mir-103-1, rno-mir-107, rno-mir-122, rno-mir-125a, rno-mir-125b-1, rno-mir-125b-2, rno-mir-126a, rno-mir-127, rno-mir-129-1, rno-mir-139, rno-mir-143, rno-mir-145, rno-mir-146a, rno-mir-206, rno-mir-221, rno-mir-222, rno-mir-223, hsa-mir-196b, mmu-mir-196b, rno-mir-196b-1, hsa-mir-20b, hsa-mir-451a, mmu-mir-451a, rno-mir-451, hsa-mir-486-1, hsa-mir-499a, mmu-mir-486a, mmu-mir-20b, rno-mir-20b, rno-mir-499, mmu-mir-499, mmu-mir-708, hsa-mir-708, rno-mir-17-2, rno-mir-708, hsa-mir-103b-1, hsa-mir-103b-2, mmu-mir-486b, hsa-mir-451b, hsa-mir-499b, mmu-mir-145b, mmu-mir-21b, mmu-let-7j, mmu-mir-130c, mmu-mir-21c, mmu-mir-451b, mmu-let-7k, hsa-mir-486-2, mmu-mir-129b, mmu-mir-126b, rno-let-7g, rno-mir-148a, rno-mir-196b-2, rno-mir-486
E [2] decreased miR-146a, miR 125a, miR-125b, let-7e, miR-126, miR-145, and miR-143 and increased miR-223, miR-451, miR-486, miR-148a, miR-18a, and miR-708 expression in mouse splenic lymphocytes [199]. [score:3]
More recently, patients whose breast tumors showed reduced miR-126, miR-206, or miR-335 were found to have reduced survival, regardless of ERα or ErbB2 status [18]. [score:1]
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[+] score: 4
Recently, a functional role of miR-126 has been suggested to be involved in dopamine neuronal cell survival in mo dels of Parkinson’s disease (PD) -associated toxicity [19]. [score:3]
Kim W MiR-126 regulates growth factor activities and vulnerability to toxic insult in neuronsMol. [score:1]
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34
[+] score: 4
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-17, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-29a, hsa-mir-30a, hsa-mir-31, hsa-mir-32, hsa-mir-33a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-106a, mmu-let-7g, mmu-let-7i, mmu-mir-27b, mmu-mir-30a, mmu-mir-30b, mmu-mir-126a, mmu-mir-9-2, mmu-mir-135a-1, mmu-mir-137, mmu-mir-140, mmu-mir-150, mmu-mir-155, mmu-mir-24-1, mmu-mir-193a, mmu-mir-194-1, mmu-mir-204, mmu-mir-205, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-143, mmu-mir-30e, hsa-mir-34a, hsa-mir-204, hsa-mir-205, hsa-mir-222, mmu-let-7d, mmu-mir-106a, mmu-mir-106b, hsa-let-7g, hsa-let-7i, hsa-mir-27b, hsa-mir-30b, hsa-mir-135a-1, hsa-mir-135a-2, hsa-mir-137, hsa-mir-140, hsa-mir-143, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-126, hsa-mir-150, hsa-mir-193a, hsa-mir-194-1, mmu-mir-19b-2, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, mmu-mir-200a, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-15a, mmu-mir-23a, mmu-mir-24-2, mmu-mir-29a, mmu-mir-31, mmu-mir-92a-2, mmu-mir-34a, rno-mir-322-1, mmu-mir-322, rno-let-7d, rno-mir-329, mmu-mir-329, rno-mir-140, rno-mir-350-1, mmu-mir-350, hsa-mir-200c, hsa-mir-155, mmu-mir-17, mmu-mir-25, mmu-mir-32, mmu-mir-200c, mmu-mir-33, mmu-mir-222, mmu-mir-135a-2, mmu-mir-19b-1, mmu-mir-92a-1, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-7b, hsa-mir-194-2, mmu-mir-194-2, hsa-mir-106b, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-30e, hsa-mir-375, mmu-mir-375, mmu-mir-133b, hsa-mir-133b, rno-let-7a-1, rno-let-7a-2, rno-let-7b, rno-let-7c-1, rno-let-7c-2, rno-let-7e, rno-let-7f-1, rno-let-7f-2, rno-let-7i, rno-mir-7b, rno-mir-9a-1, rno-mir-9a-3, rno-mir-9a-2, rno-mir-17-1, rno-mir-19b-1, rno-mir-19b-2, rno-mir-23a, rno-mir-24-1, rno-mir-24-2, rno-mir-25, rno-mir-27b, rno-mir-29a, rno-mir-30c-1, rno-mir-30e, rno-mir-30b, rno-mir-30d, rno-mir-30a, rno-mir-30c-2, rno-mir-31a, rno-mir-32, rno-mir-33, rno-mir-34a, rno-mir-92a-1, rno-mir-92a-2, rno-mir-106b, rno-mir-126a, rno-mir-135a, rno-mir-137, rno-mir-143, rno-mir-150, rno-mir-193a, rno-mir-194-1, rno-mir-194-2, rno-mir-200c, rno-mir-200a, rno-mir-204, rno-mir-205, rno-mir-222, hsa-mir-196b, mmu-mir-196b, rno-mir-196b-1, mmu-mir-410, hsa-mir-329-1, hsa-mir-329-2, mmu-mir-470, hsa-mir-410, hsa-mir-486-1, hsa-mir-499a, rno-mir-133b, mmu-mir-486a, hsa-mir-33b, rno-mir-499, mmu-mir-499, mmu-mir-467d, hsa-mir-891a, hsa-mir-892a, hsa-mir-890, hsa-mir-891b, hsa-mir-888, hsa-mir-892b, rno-mir-17-2, rno-mir-375, rno-mir-410, mmu-mir-486b, rno-mir-31b, rno-mir-9b-3, rno-mir-9b-1, rno-mir-9b-2, hsa-mir-499b, mmu-let-7j, mmu-mir-30f, mmu-let-7k, hsa-mir-486-2, mmu-mir-126b, rno-mir-155, rno-let-7g, rno-mir-15a, rno-mir-196b-2, rno-mir-322-2, rno-mir-350-2, rno-mir-486, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
Similarly, within the differentially expressed pool of miRNAs, 10 were identified that are intimately involved in regulating intracellular trafficking pathways, including: miR-7b-5p, miR-9-5p, miR-31-5p, miR-92a-3p, miR-106-5p, miR-126-3p, miR-150-5p, miR-204-5p, miR-222-3p, and miR-322-5p (S2 Fig). [score:4]
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[+] score: 4
Recent studies also indicate that a panel of miRNAs (i. e., miR-10, miR-15b, miR-16, miR-20a, miR-20b, miR-27a, miR-126, miR-145, miR-195, miR-205, and miR-210) is involved in the regulation of VEGF expression in ECs and tumor cells [16]– [26]. [score:4]
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[+] score: 4
Included among the 46 miRNAs with increased expression were 7 (miR-21, miR-16, miR-26a, miR-26b, miR-23a, miR-23b, miR-126) included in surveys of the most abundant miRNAs in human platelets [23, 24] and the miR-126 gene products miR-126-3p and miR-126-5p that are also enriched in vascular endothelial cells and endothelial microparticles [25]. [score:3]
Among the individual miRNAs previously associated with endothelial cell and monocyte activation and sepsis in humans and rodents [27– 29], we found increases in our study of miR-16, miR-21, miR-126, miR-146a, miR-150, miR-511, and miR-23b. [score:1]
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37
[+] score: 4
Bai Y. Bai X. Wang Z. Zhang X. Ruan C. Miao J. MicroRNA-126 inhibits ischemia -induced retinal neovascularization via regulating angiogenic growth factors Exp. [score:3]
Related reports by Shen and Bai et al. revealed that alteration of miRNAs such as miR-126, miR-451, miR-199a, et al., contributed to the retinal neovascularization, which is consistent with our results [17, 18]. [score:1]
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[+] score: 3
Among the 12 selected miRNAs, two were lung-specific (miR-195 and miR-200c), one was kidney-specific (miR-10a), and three were co-expressed in the lung and heart (miR-126, miR-143 and miR-145) as determined by HSD, OSI and two-fold criteria. [score:3]
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To test whether the anti-inflammatory effects of D-4F are related to miR expression, expression of miRs (miR-124a, miR-126, miR-146a, miR-153, miR-155) related to inflammation, BBB integrity and DM were measured in the ischemic brain of control and D-4F treated T1DM stroke rats. [score:3]
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40
[+] score: 3
Other miRNAs from this paper: hsa-mir-223, hsa-mir-126, rno-mir-126a, rno-mir-223
A microRNA -based approach with target sequences for EC-specific miR-126-3p at the 3′ end demonstrated this finding. [score:3]
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41
[+] score: 3
Validation of a selected few by qPCR identified 10 miRNAs - miR-133b-3p, miR-208b-3p, miR-21-5p, miR-125a-5p, miR-125b-5p, miR-126-3p, miR-210-3p, miR-29a-3p, miR-494-3p and miR-320a, that were significantly up-regulated in HF myocardium compared to normal controls. [score:3]
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42
[+] score: 3
Circulating miR-208a and miR-126 were found to be significantly and consistently altered in the plasma under different cardiac pathological conditions, like acute myocardial infarction, heart failure and coronary artery disease [13]. [score:3]
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43
[+] score: 3
Swimming training in rats increases cardiac microRNA-126 expression and angiogenesis. [score:3]
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44
[+] score: 3
Further we found that expression of four miRNAs (miR-20a, miR-98, miR-107 and miR-126) showed a trend similar to that observed in microarray but was not statistically significant (Figure 3). [score:3]
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45
[+] score: 3
Yan J. Dang Y. Liu S. Zhang Y. Zhang G. LncRNA HOTAIR promotes cisplatin resistance in gastric cancer by targeting miR-126 to activate the PI3K/AKT/MRP1 genesTumour Biol. [score:3]
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46
[+] score: 3
In addition, Hua et al. have found that Wnt4 signaling induced VSMC proliferation and was associated with intimal thickening by regulating miR-126 [16]. [score:2]
Hua J. Y. He Y. Z. Xu Y. Jiang X. H. Ye W. Pan Z. M. Emodin prevents intima thickness via Wnt4/Dvl-1/β-catenin signalingpathway mediated by miR-126 in balloon-injured carotid artery rats Exp. [score:1]
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47
[+] score: 2
Other miRNAs from this paper: hsa-mir-125a, hsa-mir-126, rno-mir-125a, rno-mir-126a
Chitosan wound dressings incorporating exosomes derived from MicroRNA-126 -overexpressing synovium mesenchymal stem cells provide sustained release of exosomes and heal full-thickness skin defects in a diabetic rat mo del. [score:2]
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48
[+] score: 2
Zampetaki A. Kiechl S. Drozdov I. Willeit P. Mayr U. Prokopi M. Mayr A. Weger S. Oberhollenzer F. Bonora E. Plasma microRNA profiling reveals loss of endothelial miR-126 and other microRNAs in type 2 diabetes Circ. [score:1]
Furthermore, plasma miRNA profiling of T2D patients showed loss of endothelial miR-126, probably resulting in impaired peripheral angiogenic signaling [19]. [score:1]
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49
[+] score: 1
miR-21, a marker of vascular smooth muscle cell proliferation and apoptosis, was also included along with miR-126, an endothelial marker, and miR-320, which is linked to ischemia and infarction [24- 26]. [score:1]
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50
[+] score: 1
We found four microRNAs (LET-7, MIR-100, MIR-125, and MIR-126) that could detect teratomas and had previously been associated with oncogenic transformations (Gu et al., 2015, Wu et al., 2015). [score:1]
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[+] score: 1
Plasma microrna profiling reveals loss of endothelial mir-126 and other micrornas in type 2 diabetes. [score:1]
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[+] score: 1
The renoprotective effect was lost if microvesicles were pre -treated with RNAse, or if the pro-angiogenic microRNAs, miR-126 and miR-296, were depleted. [score:1]
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[+] score: 1
Other miRNAs from this paper: rno-mir-21, rno-mir-126a, rno-mir-192, rno-mir-210, rno-mir-155
In a study of atherosclerosis, the delivery of miR-126 by endothelial cell-derived apoptotic bodies was found to be able to induce CXCL -dependent vascular protection [24], indicating that upon injury, apoptosis was switched on and miRNAs could be secreted into extracellular space or circulation in apoptotic bodies. [score:1]
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[+] score: 1
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-mir-18a, hsa-mir-21, hsa-mir-23a, hsa-mir-26a-1, hsa-mir-30a, hsa-mir-99a, hsa-mir-103a-2, hsa-mir-103a-1, mmu-mir-1a-1, mmu-mir-23b, mmu-mir-30a, mmu-mir-99a, mmu-mir-126a, mmu-mir-9-2, mmu-mir-133a-1, mmu-mir-138-2, hsa-mir-192, mmu-mir-204, mmu-mir-122, hsa-mir-204, hsa-mir-1-2, hsa-mir-23b, hsa-mir-122, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-138-2, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-126, hsa-mir-138-1, mmu-mir-192, mmu-let-7a-1, mmu-let-7a-2, mmu-mir-18a, mmu-mir-21a, mmu-mir-23a, mmu-mir-26a-1, mmu-mir-103-1, mmu-mir-103-2, hsa-mir-1-1, mmu-mir-1a-2, mmu-mir-26a-2, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-138-1, hsa-mir-26a-2, hsa-mir-376c, hsa-mir-381, mmu-mir-381, mmu-mir-133a-2, rno-let-7a-1, rno-let-7a-2, rno-mir-9a-1, rno-mir-9a-3, rno-mir-9a-2, rno-mir-18a, rno-mir-21, rno-mir-23a, rno-mir-23b, rno-mir-26a, rno-mir-30a, rno-mir-99a, rno-mir-103-2, rno-mir-103-1, rno-mir-122, rno-mir-126a, rno-mir-133a, rno-mir-138-2, rno-mir-138-1, rno-mir-192, rno-mir-204, mmu-mir-411, hsa-mir-451a, mmu-mir-451a, rno-mir-451, hsa-mir-193b, rno-mir-1, mmu-mir-376c, rno-mir-376c, rno-mir-381, hsa-mir-574, hsa-mir-652, hsa-mir-411, bta-mir-26a-2, bta-mir-103-1, bta-mir-16b, bta-mir-18a, bta-mir-21, bta-mir-99a, bta-mir-126, mmu-mir-652, bta-mir-138-2, bta-mir-192, bta-mir-23a, bta-mir-30a, bta-let-7a-1, bta-mir-122, bta-mir-23b, bta-let-7a-2, bta-let-7a-3, bta-mir-103-2, bta-mir-204, mmu-mir-193b, mmu-mir-574, rno-mir-411, rno-mir-652, mmu-mir-1b, hsa-mir-103b-1, hsa-mir-103b-2, bta-mir-1-2, bta-mir-1-1, bta-mir-133a-2, bta-mir-133a-1, bta-mir-138-1, bta-mir-193b, bta-mir-26a-1, bta-mir-381, bta-mir-411a, bta-mir-451, bta-mir-9-1, bta-mir-9-2, bta-mir-376c, bta-mir-1388, rno-mir-9b-3, rno-mir-9b-1, rno-mir-9b-2, hsa-mir-451b, bta-mir-574, bta-mir-652, mmu-mir-21b, mmu-mir-21c, mmu-mir-451b, bta-mir-411b, bta-mir-411c, mmu-mir-126b, rno-mir-193b, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
For example, the stem-loop sequence of bta-miR-126 was perfectly matched to those from human, mouse and rat; however, in cattle and mouse, both strands were observed as mature miRNAs, while in human and rat, one strand generates miRNA and the other strand generates miRNA*. [score:1]
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Comparison of the qPCR and Nanostrings data revealed agreement for miR-1, miR-126, and miR-17, which were unchanged after SCI by both methods (Fig 2, Tables 1 and S1). [score:1]
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56
[+] score: 1
Recent research reveals that miRNAs are involved in the pathologic process of SAP, in which miR-126a and miR-126b 43, 44 have been taken as the diagnostic markers. [score:1]
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57
[+] score: 1
Recently, miRNAs have also been recognized as novel biomarkers for early diagnosis of AMI, including miR-208α, miR-1 and miR-126 [6, 7]. [score:1]
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58
[+] score: 1
Additionally all reads of sequences originally reported in miRbase as the minor strand (*) were grouped (upon similar criteria as above; Table S5) resulting in a further 58 miRNAs of interest, 16 of which (including miR-126*, miR-140*, miR-151* and miR-28*) were detected between 1.23 and 99.56 fold higher in the * form than the ‘major’ mature sequence, while miR-501* was not detected in the major mature strand form. [score:1]
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For example, Bijkerk et al. miR-126 protect renal ischemia/reperfusion injury by promoting vascular integrity [8]. [score:1]
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This association was mainly contributed by miR-125b and miR-126. [score:1]
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61
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TCA cycle intermediates including citrate, succinate, 2-oxoglutarate and fumarate are positively correlated with miR-143, miR-126-3p, miR-146a, miR-150 and miR-155. [score:1]
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Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-16-1, hsa-mir-17, hsa-mir-21, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-30a, hsa-mir-31, hsa-mir-96, hsa-mir-99a, hsa-mir-16-2, hsa-mir-30c-2, hsa-mir-30d, hsa-mir-182, hsa-mir-183, hsa-mir-211, hsa-mir-217, hsa-mir-218-1, hsa-mir-218-2, hsa-mir-221, hsa-mir-222, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-23b, hsa-mir-30b, hsa-mir-125b-1, hsa-mir-132, hsa-mir-143, hsa-mir-145, hsa-mir-191, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-184, hsa-mir-190a, hsa-mir-195, rno-mir-322-1, rno-let-7d, rno-mir-335, rno-mir-342, rno-mir-135b, hsa-mir-30c-1, hsa-mir-299, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-379, hsa-mir-382, hsa-mir-342, hsa-mir-135b, hsa-mir-335, rno-let-7a-1, rno-let-7a-2, rno-let-7b, rno-let-7c-1, rno-let-7c-2, rno-let-7e, rno-let-7f-1, rno-let-7f-2, rno-let-7i, rno-mir-15b, rno-mir-16, rno-mir-17-1, rno-mir-21, rno-mir-23a, rno-mir-23b, rno-mir-24-1, rno-mir-24-2, rno-mir-25, rno-mir-26a, rno-mir-26b, rno-mir-30c-1, rno-mir-30e, rno-mir-30b, rno-mir-30d, rno-mir-30a, rno-mir-30c-2, rno-mir-31a, rno-mir-96, rno-mir-99a, rno-mir-125a, rno-mir-125b-1, rno-mir-125b-2, rno-mir-126a, rno-mir-132, rno-mir-143, rno-mir-145, rno-mir-183, rno-mir-184, rno-mir-190a-1, rno-mir-191a, rno-mir-195, rno-mir-211, rno-mir-217, rno-mir-218a-2, rno-mir-218a-1, rno-mir-221, rno-mir-222, rno-mir-299a, hsa-mir-384, hsa-mir-20b, hsa-mir-409, hsa-mir-412, hsa-mir-489, hsa-mir-494, rno-mir-489, rno-mir-412, rno-mir-543, rno-mir-542-1, rno-mir-379, rno-mir-494, rno-mir-382, rno-mir-409a, rno-mir-20b, hsa-mir-542, hsa-mir-770, hsa-mir-190b, hsa-mir-543, rno-mir-466c, rno-mir-17-2, rno-mir-182, rno-mir-190b, rno-mir-384, rno-mir-673, rno-mir-674, rno-mir-770, rno-mir-31b, rno-mir-191b, rno-mir-299b, rno-mir-218b, rno-mir-409b, rno-let-7g, rno-mir-190a-2, rno-mir-322-2, rno-mir-542-2, rno-mir-542-3
These include rno-miR-195, rno-miR-125a-5p, rno-let-7a, rno-miR-16, rno-miR-30b-5p, rno-let-7c, rno-let-7b, rno-miR-125b-5p, rno-miR-221, rno-miR-222, rno-miR-26a, rno-miR-322, rno-miR-23a, rno-miR-191, rno-miR-30 family, rno-miR-21, rno-miR-126, rno-miR-23b, rno-miR-145 and rno-miR-494. [score:1]
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On the other hand, both EEP and Pn significantly inhibited in a dose -dependent manner the activation of HIF1 α. Finally, VEGF mRNA and microRNAs associated with angiogenesis in previous studies (miR-126, miR-19b, miR-221, miR-222, miR-27b, and miR-17) were evaluated by real-time PCR. [score:1]
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