MiR-27 alleviates myocardial cell damage induced by hypoxia/reoxygenation via targeting TGFBR1 and inhibiting NF-κB pathway.

MiR-27 prevents atherosclerosis by inhibiting inflammatory responses induced by lipoprotein lipase. Overexpression of miR-27b attenuates angiotensin-induced atrial fibrosis. Nevertheless, studies have rarely investigated on the effect of miR-27 in cardiomyocyte injury. H9c2 cells were transfected with miR-27 mimic/inhibitor. Then the cell proliferation was tested by MTT assay and the cell apoptosis was detected by flow cytometry. The luciferase activity assay was utilized to analyze the relationship between miR-27 and TGFBR1. Quantificational real-time polymerase chain reaction and western blot were utilized to detect the cardiomyocyte differentiation marker and nuclear factor kappa B (NF-κB) pathway. Our outcomes demonstrated that miR-27 expression was downregulated cardiomyocyte injury subjected to hypoxia/reoxygenation (H/R). Additionally, overexpression of miR-27 could significantly alleviate cardiomyocyte injury by regulating cell activity and apoptosis. The luciferase activity assay confirmed that transforming growth factor ß receptor 1 (TGFBR1) is a direct hallmark of miR-27. Besides, overexpression of miR-27 promoted the expression of TGFBR1 in H/R model. After transfection with miR-27 mimic/inhibitor, the expression of NF-κB pathway-related proteins was decreased/increased. Taken together, our data manifested that miR-27 repressed cardiomyocyte injury induced by H/R via mediating TGFBR1 and inhibiting NF-κB signaling pathway. Furthermore, miR-27/ TGFBR1 might be utilized as hopeful biomarkers for myocardial ischemia diagnosis and treatment.