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Published on: June 15, 2018
miR-23a Regulates Cardiomyocyte Apoptosis by Targeting Manganese Superoxide Dismutase
Bo Long1, Tian-Yi Gan2, Rong-Cheng Zhang2
1Central Research Laboratory, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100730, China.
Abstract:
Cardiomyocyte apoptosis is initiated by various cellular insults and accumulated cardiomyocyte apoptosis leads to the pathogenesis of heart failure. Excessive reactive oxygen species (ROS) provoke apoptotic cascades. Manganese superoxide dismutase (MnSOD) is an important antioxidant enzyme that converts cellular ROS into harmless products. In this study, we demonstrate that MnSOD is down-regulated upon hydrogen peroxide treatment or ischemia/reperfusion (I/R) injury. Enhanced expression of MnSOD attenuates cardiomyocyte apoptosis and myocardial infarction induced by I/R injury. Further, we show that miR-23a directly regulates the expression of MnSOD. miR-23a regulates cardiomyocyte apoptosis by suppressing the expression of MnSOD. Our study reveals a novel model regulating cardiomyocyte apoptosis which is composed of miR-23a and MnSOD. Our study provides a new method to tackling apoptosis related cardiac diseases.
Insights
This study reveals that microRNA-23a (miR-23a) suppresses Manganese Superoxide Dismutase (MnSOD), a key antioxidant enzyme. Down-regulating miR-23a protects against heart failure by enhancing MnSOD and reducing cardiomyocyte apoptosis.
Area of Science:
- Molecular Biology
- Cardiovascular Research
- Cellular Signaling
Background:
- Cardiomyocyte apoptosis contributes to heart failure pathogenesis.
- Excessive reactive oxygen species (ROS) trigger apoptotic pathways.
- Manganese superoxide dismutase (MnSOD) is a critical ROS-scavenging enzyme.
Purpose of the Study:
- To investigate the role of MnSOD in cardiomyocyte apoptosis.
- To identify regulatory mechanisms of MnSOD expression.
- To elucidate the involvement of microRNAs in cardiac apoptosis.
Main Methods:
- Investigated MnSOD expression under oxidative stress (hydrogen peroxide) and ischemia/reperfusion (I/R) injury.
- Assessed the impact of MnSOD overexpression on I/R-induced myocardial damage.
- Determined the direct regulatory relationship between miR-23a and MnSOD at the molecular level.
Main Results:
- MnSOD expression was found to be downregulated following hydrogen peroxide treatment and I/R injury.
- Enhanced MnSOD expression significantly attenuated cardiomyocyte apoptosis and myocardial infarction.
- miR-23a was identified as a direct negative regulator of MnSOD, suppressing its expression and promoting cardiomyocyte apoptosis.
Conclusions:
- A novel regulatory axis involving miR-23a and MnSOD in controlling cardiomyocyte apoptosis was uncovered.
- Targeting the miR-23a/MnSOD pathway offers a potential therapeutic strategy for apoptosis-related cardiac diseases.
- This finding provides new insights into the molecular mechanisms underlying heart failure.
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