W-Y Liu1, H-H Sun, P-F Sun. 1. Department of Cardiovascular Surgery, The Affiliated Yantai Yuhuangding Hospital of Qingdao University, Yantai, China. spfsunny@126.com.
Abstract
OBJECTIVE: To elucidate the role of microRNA-378-containing microvesicles (MVs) in the process of myocardial fibrosis and its underlying mechanism. MATERIALS AND METHODS: In vivo chronic myocardial fibrosis (MF) model in rats was established by aortic coarctation method. MicroRNA-378 mimic or inhibitor was injected into the rat tail vein at day 3 after the aortic coarctation. Two weeks later, rats were sacrificed for collecting myocardium. MVs were isolated from rat cardiomyocytes and further verified by detecting the expression level of its marker CD63. Expression levels of fibrosis-related indicators and microRNA-378 in MVs were determined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) and Western blot. After induction with transforming growth factor-β1 (TGF-β1) in primary rat cardiomyocytes for different time points, expression levels of fibrosis-related indicators and microRNA-378 were also accessed. Changes in mitogen-activated protein kinase (MAPK) pathway were observed during the process of MF by qRT-PCR and Western blot. RESULTS: Expression levels of microRNA-378-containing MVs decreased, and the MAPK pathway was activated during the process of MF, which further aggravated MF. CONCLUSIONS: MicroRNA-378-containing MVs alleviate myocardial fibrosis through inhibiting the phosphorylation of MAPK.
OBJECTIVE: To elucidate the role of microRNA-378-containing microvesicles (MVs) in the process of myocardial fibrosis and its underlying mechanism. MATERIALS AND METHODS: In vivo chronic myocardial fibrosis (MF) model in rats was established by aortic coarctation method. MicroRNA-378 mimic or inhibitor was injected into the rat tail vein at day 3 after the aortic coarctation. Two weeks later, rats were sacrificed for collecting myocardium. MVs were isolated from rat cardiomyocytes and further verified by detecting the expression level of its marker CD63. Expression levels of fibrosis-related indicators and microRNA-378 in MVs were determined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) and Western blot. After induction with transforming growth factor-β1 (TGF-β1) in primary rat cardiomyocytes for different time points, expression levels of fibrosis-related indicators and microRNA-378 were also accessed. Changes in mitogen-activated protein kinase (MAPK) pathway were observed during the process of MF by qRT-PCR and Western blot. RESULTS: Expression levels of microRNA-378-containing MVs decreased, and the MAPK pathway was activated during the process of MF, which further aggravated MF. CONCLUSIONS: MicroRNA-378-containing MVs alleviate myocardial fibrosis through inhibiting the phosphorylation of MAPK.