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miR-190a-5p regulates cardiomyocytes response to ferroptosis via directly targeting GLS2
Xiaodao Zhou1, Mali Zhuo2, Yayun Zhang2
1Department of Anesthesiology, Ningbo Urology and Nephrology Hospital, Ningbo Yinzhou No 2. Hospital, 998 North Qianhe Road, Yinzhou District, Ningbo, 315100, Zhejiang, China.
Abstract:
Ferroptosis is a novel identified form of regulated cell death that has been implied in the pathology of myocardial infarction (MI). However, the regulation mechanisms of ferroptosis in cardiomyocyte are still elusive. MiRNAs are a group of small non-coding RNAs that play crucial roles in various biological activities. Till now, little is known about the role of miRNA in the ferroptosis of cardiomyocytes. In the current study, we found that miR-190a-5p negatively regulate ferroptosis via directly targeting GLS2 in rat cardiomyocyte H9c2 cells. Forced expression of miR-190a-5p inhibited GLS2, resulting in downregulation of ROS, MDA and Fe 2+ accumulation. Meanwhile, inhibition of miR-190a-5p caused upregulation of GLS2, resulting in opposite effects which could be blocked by GLS2 inhibitor compound 968. In summary, our findings suggest that miR-190a-5p plays an essential role in regulation of ferroptosis of cardiomyocytes and suggest a potential therapeutic target for MI.
Insights
MicroRNAs regulate ferroptosis, a cell death form implicated in myocardial infarction. This study identifies miR-190a-5p as a key regulator of ferroptosis in cardiomyocytes by targeting GLS2, offering a potential therapeutic avenue for heart attack.
Area of Science:
- Cardiovascular Biology
- Cell Death Mechanisms
- Molecular Regulation
Background:
- Ferroptosis, a regulated cell death, is implicated in myocardial infarction (MI) pathology.
- Mechanisms of ferroptosis in cardiomyocytes remain largely unknown.
- The role of microRNAs (miRNAs) in cardiomyocyte ferroptosis is poorly understood.
Purpose of the Study:
- To investigate the role of microRNAs in regulating ferroptosis in cardiomyocytes.
- To identify specific miRNAs involved in ferroptosis pathways within cardiac cells.
- To elucidate the molecular targets and mechanisms underlying miRNA-mediated ferroptosis regulation.
Main Methods:
- Utilized rat cardiomyocyte H9c2 cell line.
- Manipulated miR-190a-5p expression (forced expression and inhibition).
- Assessed GLS2 expression, reactive oxygen species (ROS), malondialdehyde (MDA), and iron (Fe 2+) accumulation.
- Employed a GLS2 inhibitor (compound 968) to validate findings.
Main Results:
- miR-190a-5p was found to negatively regulate ferroptosis in H9c2 cells.
- Forced miR-190a-5p expression inhibited GLS2, decreasing ROS, MDA, and Fe 2+.
- Inhibition of miR-190a-5p upregulated GLS2, leading to increased ferroptosis markers, which was reversible with a GLS2 inhibitor.
Conclusions:
- miR-190a-5p plays a critical role in the regulation of cardiomyocyte ferroptosis.
- The miR-190a-5p/GLS2 axis is a key pathway controlling ferroptosis in cardiac cells.
- miR-190a-5p represents a potential therapeutic target for myocardial infarction.
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