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10.18632/oncotarget.13048 http://scihub22266oqcxt.onion/10.18632/oncotarget.13048 C5346642!5346642 !27823969     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27823969 &cmd=llinks): Failed to open stream: HTTP request failed! 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Targeting EZH1 and EZH2 contributes to the suppression of fibrosis-associated genes by miR-214-3p in cardiac myofibroblasts |pdf=|usr=}}{{27823969 }} gab.com Text Targeting EZH1 and EZH2 contributes to the suppression of fibrosis-associated genes by miR-214-3p in cardiac myofibroblasts JO: Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=27823969 #FOAvip The role of microRNA-214-3p (miR-214-3p) in cardiac fibrosis was not well illustrated. The present study aimed to investigate the expression and potential target of miR-214-3p in angiotensin II (Ang-II)-induced cardiac fibrosis. MiR-214-3p was markedly decreased in the fibrotic myocardium of a mouse Ang-II infusion model, but was upregulated in Ang-II-treated mouse myofibroblasts. Cardiac fibrosis was shown attenuated in Ang-II-infused mice received tail vein injection of miR-214-3p agomir. Consistently, miR-214-3p inhibited the expression of Col1a1 and Col3a1 in mouse myofibroblasts in vitro. MiR-214-3p could bind the 3'-UTRs of enhancer of zeste homolog 1 (EZH1) and -2, and suppressed EZH1 and -2 expressions at the transcriptional level. Functionally, miR-214-3p mimic, in parallel to EZH1 siRNA and EZH2 siRNA, could enhance peroxisome proliferator-activated receptor-? (PPAR-?) expression and inhibited the expression of Col1a1 and Col3a1 in myofibroblasts. In addition, enforced expression of EZH1 and -2, and knockdown of PPAR-? resulted in the increase of Col1a1 and Col3a1 in myofibroblasts. Moreover, the NF-?B signal pathway was verified to mediate Ang-II-induced miR-214-3p expression in myofibroblasts. Taken together, our results revealed that EZH1 and -2 were novel targets of miR-214-3p, and miR-214-3p might be one potential miRNA for the prevention of cardiac fibrosis. Twit Text FOAVip Targeting EZH1 and EZH2 contributes to the suppression of fibrosis-associated genes by miR-214-3p in cardiac myofibroblasts ????Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=27823969 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27823969 #FOAvip English Wikipedia <ref>{{Cite pmid|27823969 }}</ref> Targeting EZH1 and EZH2 contributes to the suppression of fibrosis-associated genes by miR-214-3p in cardiac myofibroblasts #MMPMID27823969 Zhu WS ; Tang CM ; Xiao Z ; Zhu JN ; Lin QX ; Fu YH ; Hu ZQ ; Zhang Z ; Yang M ; Zheng XL ; Wu SL ; Shan ZX Oncotarget 2016[Nov]; 7 (48 ): 78331-78342 PMID27823969 show ga The role of microRNA-214-3p (miR-214-3p) in cardiac fibrosis was not well illustrated. The present study aimed to investigate the expression and potential target of miR-214-3p in angiotensin II (Ang-II)-induced cardiac fibrosis. MiR-214-3p was markedly decreased in the fibrotic myocardium of a mouse Ang-II infusion model, but was upregulated in Ang-II-treated mouse myofibroblasts. Cardiac fibrosis was shown attenuated in Ang-II-infused mice received tail vein injection of miR-214-3p agomir. Consistently, miR-214-3p inhibited the expression of Col1a1 and Col3a1 in mouse myofibroblasts in vitro. MiR-214-3p could bind the 3'-UTRs of enhancer of zeste homolog 1 (EZH1) and -2, and suppressed EZH1 and -2 expressions at the transcriptional level. Functionally, miR-214-3p mimic, in parallel to EZH1 siRNA and EZH2 siRNA, could enhance peroxisome proliferator-activated receptor-? (PPAR-?) expression and inhibited the expression of Col1a1 and Col3a1 in myofibroblasts. In addition, enforced expression of EZH1 and -2, and knockdown of PPAR-? resulted in the increase of Col1a1 and Col3a1 in myofibroblasts. Moreover, the NF-?B signal pathway was verified to mediate Ang-II-induced miR-214-3p expression in myofibroblasts. Taken together, our results revealed that EZH1 and -2 were novel targets of miR-214-3p, and miR-214-3p might be one potential miRNA for the prevention of cardiac fibrosis. |3' Untranslated Regions [MESH] |Angiotensin II [MESH] |Animals [MESH] |Binding Sites [MESH] |Cardiomyopathies/chemically induced/genetics/metabolism/*prevention & control [MESH] |Cells, Cultured [MESH] |Collagen Type I, alpha 1 Chain [MESH] |Collagen Type I/genetics/metabolism [MESH] |Collagen Type III/genetics/metabolism [MESH] |Disease Models, Animal [MESH] |Enhancer of Zeste Homolog 2 Protein/genetics/*metabolism [MESH] |Fibrosis [MESH] |Gene Expression Regulation [MESH] |Male [MESH] |Mice, Inbred C57BL [MESH] |MicroRNAs/genetics/*metabolism [MESH] |Myocardium/*metabolism/pathology [MESH] |Myofibroblasts/*metabolism/pathology [MESH] |NF-kappa B/metabolism [MESH] |Oligonucleotides/genetics/metabolism [MESH] |PPAR gamma/genetics/metabolism [MESH] |Polycomb Repressive Complex 2/genetics/*metabolism [MESH] |RNA Interference [MESH] |Signal Transduction [MESH]Targeting EZH1 and EZH2 contributes to the suppression of fibrosis-ass(epmc).pdf DeepDyve Pubget Overpricing