Study of circTRRAP knockdown in acute myocardial infarction by regulating miR-323-3p/SMAD2 axis
10.13406/j.cnki.cyxb.003788
- VernacularTitle:circTRRAP敲低通过调节miR-323-3p/SMAD2轴在急性心肌梗死中的研究
- Author:
Yan XIONG
1
;
Yijia TANG
Author Information
1. 四川省医学科学院/四川省人民医院心血管内科/心血管病研究所,成都 610000
- Keywords:
circular RNA;
gene regulation;
cell apoptosis;
myocar-dial infarction
- From:
Journal of Chongqing Medical University
2025;50(4):547-556
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To investigate the specific role of circTRRAP in acute myocardial infarction(AMI).Methods:The method of hy-poxia for 24 hours was used to induce the model of myocardial infarction,and the dual-luciferase reporter assay was used to investigate the interaction between circTRRAP,SMAD2,and miR-323-3p.After knockdown and overexpression of miR-323-3p and overexpres-sion of SMAD2 through transfection with si-circTRRAP,the expression levels of proinflammatory cytokines[interkeukin-6(IL-6)and tumor necrosis factor-α(TNF-α)],oxidative stress markers[malondialdehyde(MDA)and superoxide dismutase(SOD)],and apop-totic factors[Bcl-2-associated X protein(Bax),B-cell lymphoma-2(Bcl-2),and cleaved caspase-3]were measured to investigate the role of circTRRAP,SMAD2,and miR-323-3p in myocardial infarction.Results:In the model of myocardial infarction injury,the lev-els of circTRRAP and SMAD2 were significantly increased by more than 50%,whereas there was a significant reduction in the expres-sion of miR-323-3p.The downregulation of circTRRAP led to a reduction in SMAD2 expression by promoting miR-323-3p expres-sion.SMAD2 was negatively correlated with miR-323-3p,but it was positively correlated with the expression of circTRRAP.The down-regulation of circTRRAP or SMAD2 or the upregulation of miR-323-3p could increase cell viability and reduce the apoptosis rate of cardiomyocytes.Conclusion:Downregulation of circTRRAP can inhibit inflammation and alleviate AMI via the miR-323-3p/SMAD2 axis.
