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Published on: July 10, 2019
RBM3 interacts with Raptor to regulate autophagy and protect cardiomyocytes from ischemia-reperfusion-induced injury
Nan Wang1, Limeiting Wang1, Changyan Li1
1Science and Technology Achievement Incubation Center, Kunming Medical University, Kunming, China.
Abstract:
Acute myocardial infarction (AMI) is a common disease with high morbidity and mortality worldwide. However, postinfarction pathogenesis remains unclear, and it is particularly important to identify new therapeutic targets. The RNA-binding motif protein RBM3 (also known as cold-inducible protein) is known to promote translation and is associated with tumor proliferation and neuroprotection. However, little is known about the biological effects of RBM3 on myocardial infarction. In the present study, we found that RBM3 expression was significantly upregulated in ischemia-reperfusion (I/R) condition and downregulation of RBM3 inhibited autophagy and promoted apoptosis in cardiomyocytes. We confirmed that RBM3 interacts with Raptor to regulate the autophagy pathway. Taken together, these findings illustrate the protective effects of RBM3 against I/R-induced myocardial apoptosis through the autophagy pathway.
Insights
RNA-binding motif protein RBM3 is upregulated during myocardial infarction. Downregulating RBM3 promotes apoptosis and inhibits autophagy in heart cells, highlighting RBM3
Area of Science:
- Cardiology
- Molecular Biology
- Cell Biology
Background:
- Acute myocardial infarction (AMI) presents significant global health challenges with unclear post-infarction mechanisms.
- Identifying novel therapeutic targets for AMI is crucial for improving patient outcomes.
- RNA-binding motif protein 3 (RBM3) is known for its roles in translation, tumor growth, and neuroprotection, but its function in myocardial infarction is largely unexplored.
Purpose of the Study:
- To investigate the role and biological effects of RBM3 in the context of myocardial infarction.
- To determine the impact of RBM3 on cardiomyocyte apoptosis and autophagy under ischemia-reperfusion conditions.
- To elucidate the molecular mechanisms by which RBM3 influences myocardial injury.
Main Methods:
- Assessing RBM3 expression levels in ischemia-reperfusion (I/R) models.
- Manipulating RBM3 expression to observe effects on cardiomyocyte autophagy and apoptosis.
- Investigating the interaction between RBM3 and Raptor to understand its role in regulating the autophagy pathway.
Main Results:
- RBM3 expression was significantly increased under I/R conditions.
- Downregulation of RBM3 led to the inhibition of autophagy and promotion of apoptosis in cardiomyocytes.
- RBM3 was confirmed to interact with Raptor, modulating the autophagy pathway.
Conclusions:
- RBM3 plays a protective role against ischemia-reperfusion-induced myocardial apoptosis.
- The protective effects of RBM3 are mediated through the regulation of the autophagy pathway.
- RBM3 represents a potential therapeutic target for mitigating myocardial injury following infarction.
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