ArticleJournal of cardiothoracic surgery2025
MicroRNA-221-3p targets ESR1 and downregulates SLC7A11 to exacerbate hypoxia/reoxygenation-induced cardiomyocyte injury.
Article in Journal of cardiothoracic surgery, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundmicroRNA-221-3p is highly expressed after myocardial infarction and can target regulate ESR1 expression. This study aims to investigate the effects of MicroRNA-221-3p/ESR1 on hypoxia/reoxygenation(H/R)-induced cardiomyocyte injury.
methodsestablishment of H/R H9C2 cell model; normal cultured H9C2 cells were designated as the control group. Different treatment methods were applied to H9C2 cells, including miRNA negative control (miR-con), miR-221-3p mimic, miR-221-3p inhibitor, overexpression empty vector (pcDNA-con), and ESR1 overexpression vector (pcDNA-ESR1). The effects of miR-221-3p on cell viability, ROS levels, and the expression of glutathione, 4-hydroxynonenal(4-HNE), Estrogen receptor 1(ESR1), malondialdehyde (MDA) and solute carrier family 7 member 11(SLC7A11) were examined. Mitochondrial membrane potential was assessed using JC-1 staining.
resultsmiR-221-3p is highly expressed in H/R H9C2 cells, and the miR-221-3p mimics further leads to a decrease in cell activity, a decrease in glutathione levels, an increase in 4-HNE, MDA and ROS, and a decrease in the expression of Mitochondrial membrane potential, ESR1 and SLC7A11 genes. The use of miR-221-3p inhibitors or overexpression of ESR1 can partially reverse the damage induced by the miR-221-3p mimic.
conclusionsmiR-221-3p targets ESR1 to downregulate the protein expression of SLC7A11, causing damage to H/R cardiomyocytes and potentially involving ferroptosis.
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