Abstract

Background Coronary artery disease (CAD) is a common heart disease with high incidence and mortality. Myocardial ischemia is the main type of CAD, which negatively affects health worldwide. The aim of the present study was to investigate the function and mechanism of myocardial infarction-associated transcript (MIAT) in myocardial ischemia. Methods Human cardiomyocytes (HCM) were treated with oxygen-glucose deprivation (OGD) to set the in vitro model and mouse myocardial ischemia/reperfusion (I/R) was set for in vivo model. Cell viability and apoptosis were detected by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide assay, flow cytometry, and immunofluorescence analysis. Inflammatory cytokines levels were detected by enzyme-linked immunosorbent assay. Gene and protein expressions were identified by quantitative real time-polymerase chain reaction or Western blotting. The interaction of MIAT, miR-181a-5p, and janus kinase 2 (JAK2) was identified by dual-luciferase report assay. Mouse heart tissues histopathological condition were observed by hematoxylin and eosin assays. Results Expression of MIAT and JAK2 were increased in OGD-treated HCM and mice of I/R model group, and miR-181a-5p was decreased. MIAT silencing could reverse the OGD treatment induced cell proliferation inhibition, cleaved caspase-3 and Bcl2-associated X (Bax) levels increased, while those of B-cell lymphoma-2 (Bcl-2) and mitochondria's cyt-C decreased. Besides, MIAT knockdown attenuated the OGD-induced increase of tumor necrosis factor-α, interleukin (IL)-1β, and IL-6 levels. Moreover, MIAT targeted miR-181a-5p to enhance the expression of JAK2 and signal Transducer and Activator of Transcription 3 (STAT3), and miR-181a-5p overexpression promoted proliferation, whereas it inhibited apoptosis in OGD-induced cardiomyocytes. Furthermore, the regulatory effects of MIAT knockdown in