title: Effect of miR-203 expression on myocardial fibrosis.
abstract: Cardiovascular disease is one of the diseases threatening human health. Myocardial fibrosis is a major cause of cardiovascular diseases. Studies have shown that over expression of miR-203 can inhibit the fibrosis. Therefore, in this study, the effect of differential expression of miR-203 on fibrosis of cultured mouse cardiomyocytes was investigated.
  
  
  
  Activators and inhibitors of miR-203 were designed according to the sequence of miR-203, synthesized, and transfected into mouse cardiomyocytes to establish activator group, inhibitor group, and control group. The expression levels of fibrosis-related factors including FN, CTGF, and TGF-β1 were measured by Western blot and RT-PCR 24 h and 36 h after transfection.
  
  
  
  Over-expression of miR-203 in mouse cardiomyocytes significantly decreased the expression levels of TGF-β1, CTGF, and FN in a time-dependent manner, compared with that in the control group (p <0.05). Inhibition of miR-203 expression in mouse cardiomyocytes significantly increased the expression levels of TGF-β1, CTGF, and FN 36 h after transfection, compared with that in the control group (p < 0.05). No significant differences were seen in the expression levels of TGF-β1, CTGF, and FN 24 h after transfection, compared with that in the control group (p >0.05).
  
  
  
  Over-expression of miR-203 in mouse cardiomyocytes significantly decreased the expression levels of TGF-β1, CTGF, and FN, which might be used as a detection index for prediction of fibrosis.
authors.affiliation: Department of Cardiology, Tianjin First Center Hospital, Tianjin, China. chengzhiluasd@sina.com.
authors.forename: Q
authors.initials: Q
authors.lastname: He
authors.forename: C-M
authors.initials: CM
authors.lastname: Wang
authors.forename: J-Y
authors.initials: JY
authors.lastname: Qin
authors.forename: Y-J
authors.initials: YJ
authors.lastname: Zhang
authors.forename: D-S
authors.initials: DS
authors.lastname: Xia
authors.forename: X
authors.initials: X
authors.lastname: Chen
authors.forename: S-Z
authors.initials: SZ
authors.lastname: Guo
authors.forename: X-D
authors.initials: XD
authors.lastname: Zhao
authors.forename: Q-Y
authors.initials: QY
authors.lastname: Guo
authors.forename: C-Z
authors.initials: CZ
authors.lastname: Lu
mesh_terms: D000818:Animals; D002478:Cells, Cultured; D055513:Connective Tissue Growth Factor / Q000378:metabolism; D005353:Fibronectins / Q000378:metabolism; D005355:Fibrosis; D005786:Gene Expression Regulation; D006801:Humans; D051379:Mice; D035683:MicroRNAs / Q000378:metabolism*; D009206:Myocardium / Q000473:pathology*; D032383:Myocytes, Cardiac / Q000378:metabolism*; D053773:Transforming Growth Factor beta1 / Q000378:metabolism
chemical_list: C526318:CCN2 protein, mouse; D005353:Fibronectins; C575934:MIRN203 microRNA, mouse; D035683:MicroRNAs; D053773:Transforming Growth Factor beta1; D055513:Connective Tissue Growth Factor