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This study was designed to investigate the interaction between miR\u2010129 and PTEN in MIRI. A MIRI rat model and a hypoxia reoxygenation (H\/R) H9C2 cell model were constructed to simulate myocardial infarction clinically. TTC staining, creatine kinase (CK) activity, TUNEL\/Hoechst double staining, Hoechst staining and flow cytometer were used for evaluating myocardial infarction or cell apoptosis. miR\u2010129 mimic transfection experiment and luciferase reporter gene assay were conducted for investigating the function of miR\u2010129 and the interaction between miR\u2010129 and PTEN, respectively. Real\u2010time PCR and western blotting were performed to analyze the gene expression. Compared to the control, MIRI rats presented obvious myocardial infarction, higher CK activity, increased expression of caspase\u20103 and PTEN, decreased expression of miR\u2010129, and insufficient AKT phosphorylation. Consistently, H\/R significantly increased the apoptosis of H9C2 cells, concomitant with the downregulation of miR\u2010129, upregulation of PTEN and caspase\u20103, and insufficient phosphorylation of AKT, while miR\u2010129 mimic obviously inhibited the expression of PTEN and caspase\u20103, increased the AKT phosphorylation, and decreased the cell apoptosis. Additionally, miR\u2010129 mimic obviously decreased the relative luciferase activity in H9C2 cells. To our best knowledge, this study firstly found that the low expression of miR\u2010129 accelerates the myocardial cell apoptosis by directly targeting 3\u2009<jats:sup>\u2032<\/jats:sup>UTR of PTEN. miR\u2010129 is an important biomarker for MIRI, as well as a potential therapy target.<\/jats:p>","DOI":"10.1155\/2021\/5535788","type":"journal-article","created":{"date-parts":[[2021,8,16]],"date-time":"2021-08-16T23:52:15Z","timestamp":1629157935000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":6,"title":["miR\u2010129 Attenuates Myocardial Ischemia Reperfusion Injury by Regulating the Expression of PTEN in 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