Why the study?
The study was conducted to clarify the role of miRNA-19b-3p in accelerating myocardial ischemia-reperfusion injury-induced cardiomyocyte apoptosis via PTEN downregulation in acute myocardial infarction.
Does knockdown of miRNA-19b-3p reduce apoptosis in human cardiac myocytes undergoing hypoxia/reoxygenation?
Does knockdown of miRNA-19b-3p reduce apoptosis in human cardiac myocytes undergoing hypoxia/reoxygenation?
Knockdown of miRNA-19b-3p protects human cardiac myocytes from hypoxia/reoxygenation-induced apoptosis by upregulating PTEN, suggesting a potential therapeutic target for myocardial ischemia-reperfusion injury.
Answers are grounded in this paper and cite their sources.
miRNA-19b-3p/PTEN findings in HCM cells should not alter AMI care; leaves open need for in vivo and clinical validation.
OBJECTIVE: To clarify the function of miRNA-19b-3p in accelerating myocardial ischemia-reperfusion injury- (MIRI-) induced cardiomyocyte apoptosis by downregulating gene of phosphate and tension homology deleted on chromsome ten (PTEN), thus influencing the progression of acute myocardial infarction. MATERIALS AND METHODS: miRNA-19b-3p and PTEN levels in HCM cells undergoing hypoxia/reoxygenation (H/R) were determined. Meanwhile, activities of myocardium injury markers [lactate dehydrogenase (LDH), malondialdehyde; malonic dialdehyde (MDA), superoxide dismutase (SOD), and glutathione peroxidase (GSH-PX)] in H/R-induced HCM cells were tested. Through dual-luciferase reporter gene assay, the binding between miRNA-19b-3p and PTEN was verified. Regulatory effects of miRNA-19b-3p and PTEN on apoptotic rate and apoptosis-associated gene expressions (proapoptotic protein Bcl-2 associated X protein (Bax), antiapoptotic protein B-cell lymphoma-2 (Bcl-2), and cytochrome C) in H/R-induced human cardiac myocytes (HCM) cells were examined. RESULTS: miRNA-19b-3p was upregulated, while PTEN was downregulated in H/R-induced HCM cells. Knockdown of miRNA-19b-3p decreased activities of LDH, MDA, and GSH-PX, but increased SOD level in H/R-induced HCM cells. The binding between miRNA-19b-3p and PTEN was confirmed. More importantly, knockdown of miRNA-19b-3p reduced apoptotic rate, downregulated proapoptosis gene expressions (Bax and cytochrome C), and upregulated antiapoptosis gene expression (Bcl-2), which were reversed by silence of PTEN. CONCLUSIONS: miRNA-19b-3p is upregulated in HCM cells undergoing hypoxia and reoxygenation, which accelerates MIRI-induced cardiomyocyte apoptosis through downregulating PTEN.
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Li et al. (2021) studied this question.
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