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Murine Myocardial Infarction Model using Permanent Ligation of Left Anterior Descending Coronary Artery
Published on: August 16, 2019
Mechanism study of miR-324-3p driving myocardial infarction progression through regulation of myocardial inflammation
Hongxia Liu1, Wenjing Zhu2, Wenzheng Wang3
1Department of Imaging, Tangshan Third Hospital, Jinghua Road, Guye District, Tangshan City, 063004, Hebei Province, China. liuhongxiats@163.com.
Objectives:
This study aims to analyze the expression of miR-324-3p in acute myocardial infarction (AMI), as well as its regulatory effects on inflammatory responses, oxidative stress, and cell viability in cardiomyocytes.
Method:
This study enrolled 77 AMI patients and 82 healthy controls. The serum miR-324-3p levels were detected using qRT-PCR, and their diagnostic efficacy was evaluated through ROC analysis. Then construct the H/R injury model to analyze the damage of inflammatory factors, oxidative stress, and cell viability to H9c2 cardiomyocytes. Through the combination of site prediction, luciferase reporter gene validation, and STAT3 gene rescue experiments, the critical role of STAT3 in the regulation of miR-324-3p was revealed.
Results:
In AMI patients, miR-324-3p is significantly upregulated and has high diagnostic value. Overexpression of miR-324-3p exacerbates H/R-induced inflammation, while its inhibition alleviates inflammation. Under H/R treatment, the expression of miR-324-3p increased while the expression of STAT3 decreased. Knocking down STAT3 can reverse the protective effect of the miR-324-3p inhibitor, further confirming the critical role of STAT3 in the miR-324-3p regulatory pathway.
Conclusions:
The abnormal elevation of miR-324-3p has a potential diagnostic value for AMI. miR-324-3p plays a significant role in H/R-injured cardiomyocytes by targeting and inhibiting the expression of STAT3.
