The Mirna-711-Sp1-Collagen Type I Signaling Pathway Is Involved In The Anti-Fibrosis Effect Of Pioglitazone On Post-Myocardial Infarction Cardiac Fibrosis.
Keywords
Pioglitazone,Mir-711,Cardiac Fibrosis
Abstract
The role of microRNAs in cardiac fibrosis has been widely studied, but the anti-fibrotic effect of drug-regulated microRNAs and its mechanism are still unclear. Research shows that pioglitazone can improve cardiac fibrosis and promote the expression of miR-711. This study aims to elucidate The effect and mechanism of pioglitazone on changing the expression of miR-711 after myocardial infarction. The results suggest that pioglitazone reduces the expression of type I collagen and upregulates the expression of miR-711 after myocardial infarction. In cardiac fibroblasts, pioglitazone promotes the expression of miR-711 and overexpression miR-711 inhibits the expression of type I collagen. When miR-711 is inhibited, the expression of type I collagen down-regulated by pioglitazone increases. Bioinformatics screened SP1 as the target gene of miR-711, which was verified by luciferase reporter gene experiments and Westernblot. In addition, , Pioglitazone reduces the expression of SP1 after myocardial infarction. After fibroblasts are transfected with antagomir-711, the expression of SP1 down-regulated by pioglitazone increases. This study found that the miR-711-SP1-type I collagen signaling pathway is involved in the anti-fibrosis effect of pioglitazone. effect, providing new strategies for drug research based on miRNAs.
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Original research was done by Zhao Na, Yu Haiyi, Yu Haitao, Sun Min, Zhang Youyi, Xu Ming, Gao Wei
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