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A Flow Cytometry-based Assay for Measuring Mitochondrial Membrane Potential in Cardiac Myocytes After Hypoxia/Reoxygenation
Published on: July 13, 2018
Catechin relieves hypoxia/reoxygenation-induced myocardial cell apoptosis via down-regulating lncRNA MIAT
Lin Cong1, Yisheng Su2, Dazhen Wei3
1Department of Cardiology, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, China.
Insights
Catechin protects the heart from injury by inhibiting apoptosis. It achieves this by regulating the CREB/lncRNA MIAT/Akt/Gsk-3β pathway, offering a potential therapeutic strategy for myocardial ischemia-reperfusion injury.
Area of Science:
- Cardiovascular Research
- Molecular Biology
- Cellular Biology
Background:
- Myocardial ischemia/reperfusion (MI/R) injury is a significant clinical concern.
- Catechin is known to protect the heart, but its effect on H/R-induced myocardial cell apoptosis is not well understood.
Purpose of the Study:
- To investigate the protective mechanism of catechin against H/R-induced myocardial cell apoptosis.
- To elucidate the role of the CREB/lncRNA MIAT/Akt/Gsk-3β pathway in catechin's cardioprotective effects.
Main Methods:
- Quantitative real-time PCR (qRT-PCR) for lncRNA MIAT expression.
- Cell viability assays (CCK-8) and apoptosis detection (flow cytometry) in H9C2 cells.
- Dual-luciferase reporter and ChIP assays to confirm transcription factor binding.
Main Results:
- Catechin improved cardiac function and reduced lncRNA MIAT in MI/R rats.
- Catechin inhibited H/R-induced apoptosis in H9C2 cells, an effect blunted by MIAT overexpression.
- Catechin up-regulated CREB, which suppressed MIAT expression, subsequently promoting Akt/Gsk-3β activation and reducing apoptosis.
Conclusions:
- Catechin alleviates H/R-induced myocardial cell apoptosis.
- The mechanism involves the regulation of the CREB/lncRNA MIAT/Akt/Gsk-3β pathway.
- This pathway presents a potential therapeutic target for managing MI/R injury.
Background:
Catechin protects heart from myocardial ischaemia/reperfusion (MI/R) injury. However, whether catechin inhibits H/R-induced myocardial cell apoptosis is largely unknown.
Objective:
This study aims to investigate the underlying mechanism of catechin in inhibiting the apoptosis of H/R-induced myocardial cells.
Methods:
LncRNA MIAT expression was detected by qRT-PCR. Cell viability of H9C2 cells was detected using CCK-8 assay. The apoptosis of H9C2 cells was detected by flow cytometry. The interaction between CREB and MIAT promoter regions was confirmed by dual-luciferase reporter gene assay and ChIP assay.
Results:
In MI/R rats, catechin improved heart function and down-regulated lncRNA MIAT expression in myocardial tissue. In H/R-induced H9C2 cells, catechin protected against cell apoptosis, and lncRNA MIAT overexpression attenuated this protective effect of catechin. We confirmed that transcription factor CREB could bind to MIAT promoter region, and catechin suppressed lncRNA MIAT expression through up-regulating CREB. Catechin improved mitochondrial function and relieved apoptosis through promoting Akt/Gsk-3β activation. In addition, MIAT inhibited Akt/Gsk-3β activation and promoted cell apoptosis in H/R-induced H9C2 cells. Finally, we found catechin promoted Akt/Gsk-3β activation through inhibiting MIAT expression in H/R-induced H9C2 cells.
Conclusion:
Catechin relieved H/R-induced myocardial cell apoptosis through regulating CREB/lncRNA MIAT/Akt/Gsk-3β pathway.
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