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  • Title: microRNA-181c-5p stimulates the development of coronary artery disease by targeting SIRT1.
    Author: Ma C, Zheng X, Wu X, Cheng J, Zhang K.
    Journal: Hellenic J Cardiol; 2023; 69():31-40. PubMed ID: 36243396.
    Abstract:
    OBJECTIVE: MicroRNA (miR) therapeutics is a promising approach to manage coronary artery disease (CAD). Herein, this research was aimed to explore miR-181c-5p-related mechanisms in CAD through regulating SIRT1. METHODS: A CAD mouse model was established by feeding a high-fat diet in 8-week-old ApoE-/- mice. miR-181c-5p, SIRT1, and acetylated p65 levels in mouse myocardial tissues were evaluated by RT-qPCR and Western blot. Hemodynamic parameters included the maximum rising rate of the left ventricular pressure (lv + dp/dtmax) and the time values from the onset of contraction to dp/dtmax (t-dp/dtmax), while hemorheological indices included whole blood viscosity (low shear, middle shear, or high shear), plasma viscosity, hematocrit, and platelet adhesion were measured. Tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and IL-6 were detected. Mouse pathological changes, degree of fibrosis, and cardiomyocyte apoptosis in myocardial tissues were assessed by HE, Masson, and TUNEL staining, respectively. The targeting relationship between miR-181c-5p and SIRT1 was verified by bioinformatics tools, dual luciferase reporter gene assay, and RNA pull-down assays. RESULTS: In myocardial tissue of CAD mice, miR-181c-5p and acetylated p65 were upregulated while SIRT1 was downregulated. Downregulating miR-181c-5p or upregulating SIRT1 effectively ameliorated CAD by improving hemodynamics and hemorheology and reducing inflammation, pathological changes, degree of fibrosis, and cardiomyocyte apoptosis in myocardial tissues of mice. miR-181c-5p targeted SIRT1, and overexpression of SIRT1 relieved upregulated miR-181c-5p-induced injuries in CAD mice. Regulating miR-181c-5p and SIRT1 affected the acetylation of p65. CONCLUSION: Downregulation of miR-181c-5p may ameliorate myocardial pathological changes and cardiomyocyte apoptosis in CAD by upregulating SIRT1 expression and decreasing acetylated p65 levels.
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