miR-30a attenuates cardiac fibrosis in rats with myocardial infarction by inhibiting CTGF
Liwen Chen, Qian Ji, Hao Zhu, Yizhi Ren, Zhongguo Fan, Nailiang TianExperimental and Therapeutic Medicine2018
The mechanism of miR-30a in myocardial fibrosis in rats with myocardial infarction (MI) was investigated. rAAV9-miR-30a was constructed and transfected to heart via injecting into the left ventricular cavity of MI rats. The sham operation group, control group, miR-30a group and miR-30a-NC group were established. Besides, the 3'-UTR of CTGF was inserted into luciferase expression plasmid (pMir-report), then transfected into COS1 cells. miR-30a and control miRNA were, respectively, cotransfected into COS1 cells. The expression of luciferase was detected before and after knockdown of the binding site of miR-30a and the 3'-UTR of CTGF. Four weeks after MI surgery, cardiac function was measured by color Doppler echocardiography, including short axis shortening (FS) and left ventricular ejection fraction (LVEF); the myocardial collagen volume fraction (CVF) was observed by Masson's staining; deposition of collagen I and collagen III were evaluated by immunohis- tochemical stain; using real-time PCR to detect expression levels of miR-30a and CTGF; the expression of CTGF was observed by western blotting. In MI group, cardiac function was significantly improved, while the expression levels of CVF, collagen I and III, the ratio of type I/III collagen, CTGF were significantly reduced. After knockdown the binding site of miR-30a and the 3'-UTR of CTGF, luciferase expression in COS1 cells decreased significantly. miR-30a might inhibit the expression of CTGF by directly combining with the 3'-UTR site of CTGF after MI, thereby reduce the production of collagen in myocardia, inhibit myocardial fibrosis, then improve cardiac function.