Expression and function of lncRNA ANRIL in a mouse model of acute myocardial infarction combined with type 2 diabetes mellitus.

Abstract

This study intends to explore whether lncRNA ANRIL has an influence on type 2 diabetes mellitus (T2DM) complicated with acute myocardial infarction (MI) and to further investigate the underlying mechanism. The ANRIL level in peripheral blood from patients was detected by qRT-PCR. A T2DM mouse model was established by intraperitoneal injection of streptozocin (STZ). MI was induced by ligation of the left anterior descending coronary artery. Cardiac function parameters were measured using echocardiography. Triphenyltetrazolium chloride (TTC) staining was performed to determine the infarct size, and Masson staining was conducted to delineate the area of fibrosis in the myocardium. TUNEL staining was used to detect myocardial cell apoptosis. The expression of the myocardial fibrosis-related proteins TGF-β1, collagen I and collagen III was analysed using Western blot. ANRIL was upregulated in peripheral venous blood from patients with T2DM-MI and in myocardial tissues from the established T2DM-MI model mice. Furthermore, ANRIL overexpression caused cardiac dysfunction and increased the heart/body weight rate and infarct size in the T2DM-MI mice. Moreover, ANRIL overexpression caused myocardial fibrosis and myocardial cell apoptosis, and it increased the expression of the myocardial fibrosis-related proteins TGF-β1, collagen I and collagen III in the T2DM-MI mice. However, ANRIL knockdown exerted the opposite effects. ANRIL may be involved in the progression and development of T2DM-MI, which might provide novel ideas for the prevention and treatment of cardiovascular diseases.