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Murine Myocardial Infarction Model using Permanent Ligation of Left Anterior Descending Coronary Artery
Published on: August 16, 2019
Upregulated expression of miR-1/miR-206 in a rat model of myocardial infarction
Zhi-Xin Shan1, Qiu-Xiong Lin, Yong-Heng Fu
1Research Center of Guangdong General Hospital, Guangdong Provincial Cardiovascular Institute, Guangdong Academy of Medical Sciences, Guangzhou, China.
Abstract:
MicroRNAs (miRNAs) have been increasingly reported to have important roles in diverse biological and pathological processes. We investigated miR-1 and miR-206 expression and their potential roles in a rat model of myocardial infarction (MI). miR-1 and miR-206 expression were significantly increased, and insulin-like growth factor 1 (IGF-1) protein was markedly reduced without obvious change of its mRNA level after MI induction. Position 175-196 of rat IGF-1 3'-untranslated region was identified to be required for efficient downregulation by miR-1/miR-206. IGF-1 level was reduced without changing its transcript level in rat H9C2 myoblast cells modified with miR-1 (H9C2-miR-1). In the serum withdrawal and hypoxic condition, caspase-3 activity and mitochondrial potential were significantly increased in H9C2-miR-1 cells compared with the control group, respectively (p<0.05, p<0.01). Together, our results indicate that miR-1 and miR-206 are involved in apoptotic cell death in MI by post-transcriptional repression of IGF-1.
Insights
MicroRNAs miR-1 and miR-206 increase during myocardial infarction (MI). They reduce insulin-like growth factor 1 (IGF-1) protein, promoting apoptotic cell death in heart tissue.
Area of Science:
- Molecular Biology
- Cardiovascular Biology
- Biochemistry
Background:
- MicroRNAs (miRNAs) regulate gene expression and are implicated in various biological and pathological processes.
- Myocardial infarction (MI) is a critical cardiovascular event involving complex molecular mechanisms.
- Understanding the role of specific miRNAs in MI pathogenesis is crucial for developing therapeutic strategies.
Purpose of the Study:
- To investigate the expression and function of miR-1 and miR-206 in a rat model of myocardial infarction (MI).
- To elucidate the molecular mechanism by which miR-1 and miR-206 influence myocardial cells during MI.
Main Methods:
- Induction of myocardial infarction in a rat model.
- Quantification of miR-1 and miR-206 expression levels.
- Measurement of insulin-like growth factor 1 (IGF-1) protein and mRNA levels.
- Identification of the binding site of miR-1/miR-206 on IGF-1 3'-untranslated region.
- Assessment of caspase-3 activity and mitochondrial potential in modified H9C2 myoblast cells.
Main Results:
- miR-1 and miR-206 expression significantly increased post-MI.
- Insulin-like growth factor 1 (IGF-1) protein levels were markedly reduced, while its mRNA remained unchanged.
- A specific region (175-196) in the IGF-1 3'-untranslated region was identified as crucial for miR-1/miR-206-mediated downregulation.
- In H9C2 cells expressing miR-1, serum withdrawal and hypoxia led to increased caspase-3 activity and decreased mitochondrial potential.
Conclusions:
- miR-1 and miR-206 play a significant role in the apoptotic cell death observed in myocardial infarction.
- These miRNAs exert their effect through post-transcriptional repression of insulin-like growth factor 1 (IGF-1).
- The findings highlight a novel regulatory pathway involving miRNAs in the pathophysiology of MI.