中国生物工程杂志

Objective: miR-219 mediated the development of acute myocardial infarction through the regulation mechanism of TGFBR2 and the ENDMT pathway. Methods: The expression of miR-219 in the serum of AMI patients and mice was detected by qRT-PCR. The target gene of miR-219 was screened in gene database of microRNA. The regulatory mechanism of TGFBR2 and miR-219 was examined by luciferase reporter gene and qRT-PCR.The blood scores (LVEF) of AMI mice were measured 4 weeks after myocardial injection of miR-219 lentivirus (LVEF) by cardiac echocardiography. The mRNA expression of Nppa in AMI mice injected with miR-219 lentivirus was detected by qRT-PCR. The changes of left ventricular fibrosis in mice were detected by Masson’s trichrome staining. immunohistochemical analysis of the left ventricular section of mice was performed using spla-sma. Expression levels of P-smad2, P-smad3 and TGFBR2 hypoxia induced protein phosphorylation were detected by Western blot. Results: miR-219 can regulate AMI. miR-219 inhibited the mRNA expression of TGFBR2, while miR-219 inhibitor inhibited the down-regulation effect. miR-219 can inhibit the process of acute myocardial infarction and promote the recovery of myocardial function of infarction. miR-219 can promote the angiogenesis and maturity of the myocardial tissue of AMI mice, and eventually the cardiac contractility increases and the cardiac function recovers. miR-219 can inhibit the inhibition of EndMT pathway by TGFBR2, leading to the alleviation of the pathological process of AMI. Conclusion: miR-219 can inhibit the EndMT pathway by inhibiting TGFBR2, reduce myocardial fibrosis, promote angiogenesis and maturity, recover cardiac function and inhibit the pathological development of AMI.