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MiR-208a aggravates H2O2-induced cardiomyocyte injury by targeting APC
Feng Liu1, Han Zhang2, Zhe Zhang1
1Intensive Care Unit, Huaihe Hospital of Henan University, Kaifeng, 475000, Henan, China.
Abstract:
Oxidative stress injury, inducing cardiomyocyte injury, is the major denominator of many cardiovascular diseases. In present study, we aimed to explore the molecular mechanism of microRNA-208a (miR-208a) in oxidative stress-induced cardiomyocyte injury. In this study, hydrogen peroxide (H2O2)-induced injury in H9c2 and AC16 cardiomyocytes was used as a model of myocardial injury. The pro-apoptosis potential and mechanism of miR-208a for oxidative injury were evaluated by MTT, flow cytometry, qRT-PCR and Western blot assays. Intracellular reactive oxygen species and detection of lactate dehydrogenase (LDH), malondialdehyde (MDA), and superoxide dismutase (SOD) were performed to analyze the effect of miR-208a on H2O2-induced injury in H9c2 cardiomyocytes. The association between miR-208a and activated protein C (APC) was confirmed by luciferase reporter and RIP assays. We foundthatmiR-208a mimic aggravated H2O2-induced apoptosis and oxidative injury in cardiomyocytes, while miR-208a inhibitor hadan inverse effect. APC was a target gene of miR-208a and miR-208a negatively regulated the expression of APC. APC reduced H2O2-induced injury in H9c2 cardiomyocytes. Knockdown of APC attenuated the inhibitiveeffect of miR-208a inhibitor on H2O2-induced injuryin H9c2 cardiomyocytes. We concluded thatmiR-208a could aggravate H2O2-induced injury in H9c2 cardiomyocytes by targeting APC. A new signaling pathway miR-208a/APC was first observed in myocardial injury.
Insights
MicroRNA-208a (miR-208a) worsens oxidative stress-induced cardiomyocyte injury by targeting activated protein C (APC). Inhibiting miR-208a protects heart cells from damage, revealing a new miR-208a/APC signaling pathway in myocardial injury.
Area of Science:
- Cardiovascular Biology
- Molecular Cardiology
- Oxidative Stress Research
Background:
- Oxidative stress is a key factor in cardiovascular diseases, causing cardiomyocyte injury.
- Understanding the molecular mechanisms underlying this injury is crucial for developing effective treatments.
Purpose of the Study:
- To investigate the role of microRNA-208a (miR-208a) in oxidative stress-induced cardiomyocyte injury.
- To elucidate the molecular mechanism involving miR-208a and its potential targets in myocardial injury.
Main Methods:
- Hydrogen peroxide (H₂O₂) was used to induce oxidative stress in H9c2 and AC16 cardiomyocyte cell lines.
- Cell viability (MTT), apoptosis, reactive oxygen species, lactate dehydrogenase (LDH), malondialdehyde (MDA), and superoxide dismutase (SOD) levels were assessed.
- The interaction between miR-208a and activated protein C (APC) was confirmed using luciferase reporter and RNA immunoprecipitation (RIP) assays.
Main Results:
- miR-208a mimic exacerbated H₂O₂-induced apoptosis and oxidative injury, while miR-208a inhibitor showed protective effects.
- Activated protein C (APC) was identified as a direct target gene of miR-208a, with miR-208a negatively regulating APC expression.
- APC demonstrated a protective role against H₂O₂-induced injury in cardiomyocytes, and its knockdown reversed the protective effects of the miR-208a inhibitor.
Conclusions:
- miR-208a aggravates oxidative stress-induced cardiomyocyte injury by targeting and downregulating APC.
- A novel signaling pathway, miR-208a/APC, has been identified as a significant player in the pathogenesis of myocardial injury.
