Abstract
Hypoxia-induced apoptosis and inflammation play an important role in cardiovascular diseases including myocardial infarction (MI). miR-369 has been suggested to be a key regulator of cardiac fibrosis. However, the role of miR-369 in regulating hypoxia-induced heart injury remains unknown. Our data indicated that miR-369 expression was significantly down-regulated and TRPV3 was significantly up-regulated in myocardial tissue after MI in rats and in hypoxic-treated neonatal rat cardiomyocytes (NRCMs). In addition, we observed that hypoxia significantly promoted apoptosis and the inflammatory response, accompanied by increased caspase-3 activity and the secretion of the cytokines interleukin (IL)-6, IL-1β, and tumor necrosis factor (TNF)-α. miR-369 overexpression significantly suppressed cell apoptosis and inflammatory factor production triggered by hypoxia, whereas miR-369 inhibition had an opposite effect. Importantly, we identified TRPV3 as a direct target of miR-369-3p. TRPV3 inhibition with small interfering RNA (siRNA) significantly inhibited hypoxia-induced inflammation and apoptosis, which can reverse the injury effects of miR-369 inhibitors. Our findings indicated that miR-369 reduced hypoxia-induced apoptosis and inflammation by targeting TRPV3.
Highlights
Acute myocardial infarction (MI) is the major cause of death in patients with cardiovascular disease [1]
MiR-369 expression was significantly down-regulated in ischemia/hypoxia-induced cardiomyocytes compared to the sham/control group (Figure 1C and D)
We found that TRPV3 was significantly overexpressed in myocardial cells induced by ischemia/hypoxia (Figure 1E and F)
Summary
Acute myocardial infarction (MI) is the major cause of death in patients with cardiovascular disease [1]. Growing evidence highlights the importance of inflammatory response and myocardial apoptosis in the pathogenesis of acute MI, as they are involved in mediating impaired myocardial function and heart failure [2,3]. Inflammatory cell infiltration can clear necrotic cardiomyocytes and extracellular matrix fragments to promote the healing process [2], continued inflammatory and immune infiltration is directly related to myocardial apoptosis and impairs cardiac function [4,5]. A better understanding of the regulators involved in myocardial apoptosis and inflammation is important for the exploitation of novel therapeutic targets for MI
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