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4 publications mentioning gga-mir-210b

Open access articles that are associated with the species Gallus gallus and mention the gene name mir-210b. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

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[+] score: 220
[34] We proved CTGF increases accumulation of HIF-1 α into nuclei as inhibited by miR-210 inhibitor, thus promoting HIF-1 α -dependent VEGF expression and angiogenesis by inhibiting GPD1L expression and PHD2 activity via miR-210 upregulation. [score:14]
CTGF promotes HIF-1 α -dependent VEGF expression and angiogenesis by inhibiting GPD1L expression and PHD2 activity via upregulating miR-210To identify mechanism of miR-210-involved VEGF -dependent angiogenesis, we searched for downstream genes using bioinformative screening analysis of miRNA target databank: TargetScan, MicroCosm, and miRanda. [score:14]
[35] CTGF -inhibited HIF-1 α hydroxylation was reversed by miR-210 inhibitor, leading to decrease the accumulation of HIF-1 α into nucleus (Figure 5c), indicating CTGF -mediated miR-210 upregulation inhibits PHD2 expression and subsequently increases HIF-1 α activation. [score:12]
These suggest CTGF boosting HIF-1 α -dependent VEGF expression and angiogenesis by inhibiting GPD1L expression and PHD2 activity through upregulation of miR-210. [score:10]
CTGF activates PI3K, AKT, ERK, and NF- κB/ELK1 pathway, leading to the upregulation of miR-210, contributing to inhibit the GPD1L expression and PHD2 activity, promoting the HIF-1 α -dependent VEGF expression and angiogenesis in human synovial fibroblasts (Figure 7). [score:10]
CTGF promotes HIF-1 α -dependent VEGF expression and angiogenesis by inhibiting GPD1L expression and PHD2 activity via upregulating miR-210. [score:10]
45, 46 We use miRNA target prediction (TargetScan, MicroCosm, and miRanda) to find GPD1L as most probable miR-210 target, whereas CTGF decreased GPDlL mRNA expression. [score:9]
To verify direct CTGF inducement of miR-210-mediating VEGF -dependent angiogenesis, we transfected miR-210 mimic or inhibitor into OASFs; miR-210 inhibitor but not mimic blocked CTGF -induced VEGF expression, EPC tube formation and migration (Figures 3b–d). [score:8]
We also indicated that miR-210 directly repressed GPD1L protein expression through binding to 3′UTR of human GPD1L gene, thereby negatively regulating GPD1L that is documented as promoting PHD activity and later impeding HIF-1 α expression. [score:7]
On the other hand, miR-210 inhibitor reversed CTGF -inhibited GPD1L mRNA and protein expression (Figure 5b). [score:7]
For serial experiments, cells were pretreated for 30 min with inhibitors, including Ly294002, Wortmannin, AKTi, U0126, PD98059, and HIF-1 α inhibitor or transfected with miR-210 mimic, miR-210 inhibitor, ELK1 siRNA, p65 siRNA, and CTGF shRNA for 24 h, followed by treatment with CTGF for 24 h to prevent signaling via CTGF pathway. [score:7]
Transfection of miR-210 inhibitor significantly reversed CTGF -inhibited GPD1L expression. [score:7]
With CTGF -mediated VEGF expression or EPC tube formation and migration reduced by transfection with ELK1 and p65 siRNA (Figures 4c–e), we postulate CTGF-increased miR-210 upregulation and angiogenesis as involving NF- κB and ELK1 transactivation. [score:6]
One mechanism underlying CTGF increased VEGF yield by activating PI3K, AKT, ERK, and NF- κB/ELK1 pathway, thus upregulating miR-210 expression. [score:6]
Pretreatment with PI3K (Ly294002 or Wortmannin), AKT (AKTi), and ERK inhibitors (U0126 or PD98059) for 30 min reduced CTGF -induced miR-210 expression (Figure 3f). [score:5]
These inhibitors antagonized CTGF-increased miR-210 expression, indicating CTGF-increased VEGF -dependent angiogenesis via PI3K, AKT, ERK, and miR-210 signaling pathways. [score:5]
To identify mechanism of miR-210-involved VEGF -dependent angiogenesis, we searched for downstream genes using bioinformative screening analysis of miRNA target databank: TargetScan, MicroCosm, and miRanda. [score:5]
Figure 4b shows all these inhibitors or siRNAs markedly reducing CTGF -induced miR-210 expression. [score:5]
From these three databanks overlapping between predicted targets of miR-210, GPD1L ranked as most probable target. [score:5]
We used luciferase reporter vectors harboring wild-type 3'-untranslated region (3′UTR) of GPD1L mRNA (wt-GPD1L-3′UTR) and vector containing mismatches in predicted miR-210 -binding site (full muntant-GPD1L-3′UTR) to learn if miR-210 regulates 3′UTR of GPD1L. [score:4]
Therefore, miR-210 directly represses GPD1L expression through binding to 3′UTR of human GPD1L gene. [score:4]
Among significantly regulated miRNAs, miR-210 was most upregulated in CTGF -treated OASFs compared with controls. [score:4]
Involvement of NF- κB and ELK1 in CTGF increases miR-210 upregulation. [score:4]
Involvement of NF- κB and ELK1 in CTGF increases miR-210 upregulationThe miR-210 promoter contains NF- κB- and ELK1 -binding sites. [score:4]
We screened 96 miRNAs from customized miRNA array to find miR-210 most upregulated in CTGF -treated OASFs. [score:4]
47, 48 On the other hand, PI3K, AKT, and ERK reportedly regulate miR-210 expression. [score:4]
We directly applied CTGF in OASFs to rate miR-210 expression, which miR-210 raised in a time -dependent manner (Figure 3a). [score:4]
PI3K, AKT, and ERK pathways are reported to regulate expression of miR-210 and VEGF. [score:4]
Figure 5a shows CTGF and miR-210 mimic inhibiting luciferase activity in wt-GPD1L-3′UTR plasmid but not in muntant-GPD1L-3′UTR plasmid. [score:3]
[44] We saw OASF transfection with miR-210 inhibitor reducing CTGF -induced VEGF production as well as EPC tube formation and migration, making it an angiogenic gene in human OASFs. [score:3]
[34] To determine which transcription factors are involved in CTGF -induced miR-210 expression, three different length miR-210 promoter constructs were generated. [score:3]
Also, qPCR confirmed expression of miR-210 in OASFs starkly higher than in normal SFs, indicating that miR-210 promotes angiogenesis. [score:3]
portend CTGF acting via PI3K, AKT, and ERK signaling pathways to promote miR-210 expression and VEGF -dependent angiogenesis in human synovial fibroblasts. [score:3]
31, 32, 33 We assessed their roles in CTGF -induced miR-210 and VEGF expression. [score:3]
CTGF thus increases VEGF -dependent angiogenesis by augmenting miR-210 expression through PI3K, AKT, ERK, and NF- κB/ELK1 signaling pathways in human synovial fibroblasts. [score:3]
We also found miR-210 expression in OASFs sharply higher than in normal SFs (Supplementary Figure 2). [score:3]
These suggest miR-210 as positive regulator of CTGF -mediated, VEGF -dependent angiogenesis in OASFs. [score:2]
The customized miRNA array primer was obtained from System Biology Ireland (Galway, Ireland); DMEM, α-MEM, fetal bovine serum (FBS), and all other cell culture reagents from Gibco-BRL Life Technologies (Grand Island, NY, USA); wild-type 3′UTR of GPD1L mRNA (wt-GPD1L- 3′UTR) and vector containing mismatches in predicted miR-210 -binding site (full muntant-GPD1L-3′UTR) from Addgene (Cambridge, MA); ON-TARGET plus siRNAs of ELK1, p65, GPD1L and control from Dharmacon Research (Lafayette, CO, USA); all other chemicals Sigma-Aldrich (St. [score:2]
The miR-210 promoter contains NF- κB- and ELK1 -binding sites. [score:1]
Plasmid pGL2-Basic (Promega, Madison, WI, USA) was used to generate constructs of the human miR-210 (hmiR-210) promoter. [score:1]
CTGF promotes VEGF production and angiogenesis by increasing miR-210 via PI3K, AKT, and ERK pathways. [score:1]
Pretreatment of cells with Ly294002, Wortmannin, AKTi, U0126, and PD98059 abolished CTGF-increased p-p65 and p-ELK1 accumulation into nuclei as well as p65 and ELK1 binding to NF- κB and ELK1 elements on miR-210 promoter (Figures 4f and g). [score:1]
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[+] score: 14
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-21, hsa-mir-16-2, mmu-let-7g, mmu-let-7i, mmu-mir-9-2, mmu-mir-151, mmu-mir-10b, hsa-mir-192, mmu-mir-194-1, mmu-mir-199a-1, hsa-mir-199a-1, mmu-mir-122, hsa-mir-10a, hsa-mir-10b, hsa-mir-199a-2, hsa-mir-199b, hsa-mir-210, hsa-mir-214, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-122, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-194-1, mmu-mir-192, 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-16-1, mmu-mir-16-2, mmu-mir-21a, mmu-mir-10a, mmu-mir-210, mmu-mir-214, mmu-mir-199a-2, mmu-mir-199b, mmu-mir-9-1, mmu-mir-9-3, hsa-mir-194-2, mmu-mir-194-2, hsa-mir-365a, mmu-mir-365-1, hsa-mir-365b, hsa-mir-151a, gga-let-7i, gga-let-7a-3, gga-let-7b, gga-let-7c, gga-mir-16-1, gga-mir-194, gga-mir-10b, gga-mir-199-2, gga-mir-16-2, gga-let-7g, gga-let-7d, gga-let-7f, gga-let-7a-1, gga-mir-199-1, gga-let-7a-2, gga-let-7j, gga-let-7k, gga-mir-122-1, gga-mir-122-2, gga-mir-9-2, mmu-mir-365-2, gga-mir-9-1, gga-mir-365-1, gga-mir-365-2, hsa-mir-151b, mmu-mir-744, gga-mir-21, hsa-mir-744, gga-mir-199b, gga-mir-122b, gga-mir-10a, gga-mir-16c, gga-mir-214, sma-let-7, sma-mir-71a, sma-bantam, sma-mir-10, sma-mir-2a, sma-mir-3479, sma-mir-71b, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, mmu-let-7k, gga-mir-365b, sma-mir-8437, sma-mir-2162, gga-mir-9-3, gga-mir-210a, gga-mir-9-4, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3, gga-mir-9b-1, gga-mir-10c, gga-let-7l-1, gga-let-7l-2, gga-mir-122b-1, gga-mir-9b-2, gga-mir-122b-2
Temporal expression analysis of miR-199, miR-214, miR-21, miR-210, miR-122, miR-192 and miR-194 in the liver during S. mansoni infectionBetween weeks 6 and 12, female parasites continue to produce ∼300 eggs per day [51], resulting in an increase in the number of granulomas in the liver and the development of fibrosis [45]. [score:4]
In contrast, the miRNAs up-regulated in the liver (miR-199-3p, miR-199-5p, miR-21, miR-214 and miR-210) showed significantly higher levels in mouse serum at 12 weeks post infection (Fig. 2), however these failed to differentiate S. mansoni infected from uninfected humans (Fig. S4). [score:4]
Temporal expression analysis of miR-199, miR-214, miR-21, miR-210, miR-122, miR-192 and miR-194 in the liver during S. mansoni infection. [score:3]
Consistent with the array results, there was an increase in miR-199-5p, miR-199-3p, miR-214, miR-21, miR-210, and a reduction of miR-192, miR-194, miR-365, miR-122 and miR-151 in the liver tissue of S. mansoni infected mice as compared to naïve mice; miR-9 and miR-744 did not display differential expression and were not analysed further (Table 1). [score:2]
The 5 host miRNAs were detectable in serum (miR-21, miR-199-3p, miR-199-5p, miR-210, miR-214) but showed variable abundance and failed to differentiate ‘egg -positive’ and ‘egg -negative’ participants (Fig. S4). [score:1]
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[+] score: 3
It has recently been reported that an Argonaute 2 switch regulates circulating miR-210 to coordinate hypoxic adaptation across anatomically distinct cells [63], adding to the theory that some miRNAs may be specifically secreted in the blood stream and function in intercellular communication between distant tissues [2]. [score:2]
Three of the six remaining mature miRNAs (mmu-miR-143-3p, mmu-miR-145a-5p and dre-miR-210-5p) have no sequence homology with Gallus gallus annotated miRNAs, and three (ENSGALT00000043002-5p and-3p, and ENSGALT00000042483-3p) are encoded by two miRNA genes predicted in the chicken genome (http://www. [score:1]
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[+] score: 1
miR-210 and miR-373 were discovered in HeLa and MCF-7 cells. [score:1]
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