
Study of circTRRAP knockdown in acute myocardial infarction by regulating miR-323-3p/SMAD2 axis
Xiong Yan, Tang Yijia
Study of circTRRAP knockdown in acute myocardial infarction by regulating miR-323-3p/SMAD2 axis
Objective To investigate the specific role of circTRRAP in acute myocardial infarction(AMI). Methods The method of hypoxia 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 overexpression 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 apoptotic 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 levels of circTRRAP and SMAD2 were significantly increased by more than 50%,whereas there was a significant reduction in the expression of miR-323-3p. The downregulation of circTRRAP led to a reduction in SMAD2 expression by promoting miR-323-3p expression. SMAD2 was negatively correlated with miR-323-3p,but it was positively correlated with the expression of circTRRAP. The downregulation 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.
circular RNA / gene regulation / cell apoptosis / myocardial infarction
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