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In vitro Assessment of Myocardial Protection following Hypothermia-Preconditioning in a Human Cardiac Myocytes Model
Published on: October 27, 2020
MicroRNA-369 attenuates hypoxia-induced cardiomyocyte apoptosis and inflammation via targeting TRPV3
Jinghao Wang1, Xu Chen2, Wei Huang3
1Department of Pharmacy, the First Affiliated Hospital, Jinan University, Guangzhou, China.
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.
Insights
MicroRNA-369 (miR-369) protects against heart injury from hypoxia. It reduces apoptosis and inflammation by targeting TRPV3, offering a potential therapeutic target for myocardial infarction.
Area of Science:
- Cardiovascular Biology
- Molecular Cardiology
- Cellular Stress Response
Background:
- Hypoxia-induced apoptosis and inflammation are key in cardiovascular diseases like myocardial infarction (MI).
- MicroRNA-369 (miR-369) is implicated in cardiac fibrosis, but its role in hypoxia-induced heart injury is unclear.
- TRPV3 is upregulated in myocardial tissue post-MI and in hypoxic cardiomyocytes.
Purpose of the Study:
- To investigate the role of miR-369 in hypoxia-induced heart injury.
- To identify the molecular mechanisms underlying miR-369's function in cardiac cells under hypoxic stress.
Main Methods:
- Assessed miR-369 and TRPV3 expression in rat myocardial tissue post-MI and in hypoxic neonatal rat cardiomyocytes (NRCMs).
- Evaluated the effects of miR-369 overexpression and inhibition on hypoxia-induced apoptosis and inflammation.
- Utilized small interfering RNA (siRNA) to inhibit TRPV3 and examined its impact on hypoxia-induced injury.
- Confirmed TRPV3 as a direct target of miR-369-3p.
Main Results:
- miR-369 expression was downregulated, while TRPV3 was upregulated in myocardial tissue after MI and in hypoxic NRCMs.
- Hypoxia promoted apoptosis and inflammation, evidenced by increased caspase-3 activity and elevated IL-6, IL-1β, and TNF-α.
- miR-369 overexpression attenuated hypoxia-induced apoptosis and inflammation; inhibition exacerbated these effects.
- TRPV3 inhibition reversed the detrimental effects of miR-369 inhibition on hypoxia-induced cardiac injury.
Conclusions:
- miR-369 plays a protective role against hypoxia-induced apoptosis and inflammation in the heart.
- The protective mechanism involves miR-369 targeting and downregulating TRPV3 expression.
- miR-369-3p/TRPV3 axis represents a potential therapeutic strategy for managing hypoxia-related cardiovascular diseases.
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