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10.1111/jcmm.12754 http://scihub22266oqcxt.onion/10.1111/jcmm.12754 C4759464!4759464!26756969     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Cell+Mol+Med 2016 ; 20 (3): 495-505 Nephropedia Template TP {{tp|p=26756969|t=2016. MicroRNA?503 promotes angiotensin II?induced cardiac fibrosis by targeting Apelin?13 |pdf=|usr=}}{{26756969}} gab.com Text MicroRNA 503 promotes angiotensin II induced cardiac fibrosis by targeting Apelin 13 JO: J Cell Mol Med http://www.kidney.de/pget.php?&tw=1&pmid=26756969 #FOAvip Cardiac fibrosis is a major cause of heart failure. MicroRNAs (miRs) are important epigenetic regulators of cardiac function and cardiovascular diseases, including cardiac fibrosis. This study aimed to explore the role of miR?503 and its mechanisms in regulating cardiac fibrosis. miR?503 was found up?regulated in the mouse LV tissues subjected to transverse aortic constriction (TAC) and in neonatal cardiac fibroblasts (CFs) cultured with Angiotension II. The role of miR?503 in regulating CF cell proliferation and/or collagen production in mice neonatal CFs were determined using an MTT assay and RT?PCR respectively. Forced expression of miR?503 increased the cellular proliferation and collagen production in mice neonatal CFs. The effects were abrogated by cotransfection with AMO?503 (a specific inhibitor of miR?503). Injection of antagomiR?503 elevated cardiac function and inhibited the expression of connective tissue growth factor (CTGF) and transforming growth factor (TGF)?? in the TAC mice. Additional analysis revealed that Apelin?13 is a direct target of miR?503, as the overexpression of miR?503 decreased the protein and mRNA expression levels of Apelin?13. In the CFs with pre?treatment of AngII, we transfected AMO?503 into the cells treated with siRNA?APLN. siRNA?APLN abolished the effects of AMO?503 on the production of collagen I and III and the expression of TGF?? and CTGF. Furthermore, pre?treatment of CFs with Apelin?13 (1?100 nmol/l) inhibited angiotensin II?mediated collagen production and activation of CTGF and TGF??. So we conclude that miR?503 promotes cardiac fibrosis via miR?503?Apelin?13?TGF???CTGF?collagen production pathway. Thus, miR?503 is a promising therapeutic target for reducing cardiac fibrosis. Twit Text FOAVip MicroRNA 503 promotes angiotensin II induced cardiac fibrosis by targeting Apelin 13 ????J Cell Mol Med http://www.kidney.de/pget.php?&tw=1&pmid=26756969 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26756969 #FOAvip English Wikipedia <ref>{{Cite pmid|26756969}}</ref> MicroRNA?503 promotes angiotensin II?induced cardiac fibrosis by targeting Apelin?13 #MMPMID26756969 Zhou Y; Deng L; Zhao D; Chen L; Yao Z; Guo X; Liu X; Lv L; Leng B; Xu W; Qiao G; Shan H J Cell Mol Med 2016[Mar]; 20 (3): 495-505 PMID26756969show ga Cardiac fibrosis is a major cause of heart failure. MicroRNAs (miRs) are important epigenetic regulators of cardiac function and cardiovascular diseases, including cardiac fibrosis. This study aimed to explore the role of miR?503 and its mechanisms in regulating cardiac fibrosis. miR?503 was found up?regulated in the mouse LV tissues subjected to transverse aortic constriction (TAC) and in neonatal cardiac fibroblasts (CFs) cultured with Angiotension II. The role of miR?503 in regulating CF cell proliferation and/or collagen production in mice neonatal CFs were determined using an MTT assay and RT?PCR respectively. Forced expression of miR?503 increased the cellular proliferation and collagen production in mice neonatal CFs. The effects were abrogated by cotransfection with AMO?503 (a specific inhibitor of miR?503). Injection of antagomiR?503 elevated cardiac function and inhibited the expression of connective tissue growth factor (CTGF) and transforming growth factor (TGF)?? in the TAC mice. Additional analysis revealed that Apelin?13 is a direct target of miR?503, as the overexpression of miR?503 decreased the protein and mRNA expression levels of Apelin?13. In the CFs with pre?treatment of AngII, we transfected AMO?503 into the cells treated with siRNA?APLN. siRNA?APLN abolished the effects of AMO?503 on the production of collagen I and III and the expression of TGF?? and CTGF. Furthermore, pre?treatment of CFs with Apelin?13 (1?100 nmol/l) inhibited angiotensin II?mediated collagen production and activation of CTGF and TGF??. So we conclude that miR?503 promotes cardiac fibrosis via miR?503?Apelin?13?TGF???CTGF?collagen production pathway. Thus, miR?503 is a promising therapeutic target for reducing cardiac fibrosis. äMicroRNA?503 promotes angiotensin II?induced cardiac fibrosis by targe(epmc).pdf DeepDyve Pubget Overpricing