Abstract
Myocardial infarction (MI) is a significant cause of death and disability, and sevoflurane (sevo) can protect myocardium in clinic. We aim to assess the effects of miR-210-3p on MI rats undergoing sevo treatment with the involvement of adenylyl cyclase type 9 (ADCY9). Rat MI models were constructed by ligation of the left anterior descending, and the modeled rats were respectively treated with sevo, miR-210-3p agomir, antagomir, or overexpressed ADCY9. Then, miR-210-3p and ADCY9 expression, cardiac function, myocardial injury and fibrosis, and cardiomyocyte apoptosis in rats were evaluated. Target relation between miR-210-3p and ADCY9 was detected. miR-210-3p was downregulated while ADCY9 was upregulated in MI rats. Sevo was able to promote cardiac function and attenuate myocardial injury and fibrosis, as well as cardiomyocyte apoptosis in MI rats. These effects of sevo were strengthened by miR-210-3p elevation but abolished by miR-210-3p inhibition in MI rats. The role of elevated miR-210-3p in MI rats was reversed by overexpression of ADCY9. Upregulated miR-210-3p improves sevo-induced protective effect on ventricular remodeling in rats with MI through inhibiting ADCY9.
Highlights
Myocardial infarction (MI) is mostly caused by rupture of atherosclerotic plaques leading to thrombus formation in lumen of a coronary vessel, which in turn blocks the blood flow to distal myocardium [1]
In order to explore the effect of sevo on MI, we firstly evaluated rat cardiac function using an electrocardiograph, and the results (Fig. 1A-D) indicated that left ventricle internal dimension at systole (LVIDs) and LVIDd were heightened while left ventricle ejection fraction (LVEF) and fractional shortening (FS) were lowered in the MI group versus the sham group; rats in the sevo group had suppressed LVIDs and LVIDd and elevated LVEF and FS when compared with the MI group
Cardiac function was evaluated and our results indicated that contrasted to the sevo + miR-210-3p agomir group, LVIDs and LVIDd were significantly increased, while LVEF and FS were significantly decreased in the sevo + miR-210-3p agomir + oe-adenylyl cyclase type 9 (ADCY9) group (Fig. 4C-F), showing that ADCY9 elevation abolishes the effect of sevo and miR-210-3p on improving cardiac function in MI rats
Summary
Myocardial infarction (MI) is a significant cause of death and disability, and sevoflurane (sevo) can protect myocardium in clinic. We aim to assess the effects of miR-210-3p on MI rats undergoing sevo treatment with the involvement of adenylyl cyclase type 9 (ADCY9)
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