This study aims to investigate whether miR-29c is involved in regulating transforming growth factor-β (TGF-β) mediated inflammation in diabetic cardiomyopathy (DCM). Our data showed increased inflammation and oxidative stress in diabetic myocardium together with decrease of miR-29c and elevation of TGF-β expression. In vitro experiments, we transfected miR-29c mimic and antagomir into HL-1 cells to explore the effect of miR-29c on inflammation in hyperglycemic conditions. Overexpression of miR-29c down-regulated the elevated TNF-α level, ROS production and NADPH oxidase activity which caused by high glucose. However, above changes were reversed by miR-29c antagomir. Interestingly, TGF-β protein rather than mRNA expression was changed significantly after transfection with miR-29c mimic, indicating that the modulation of TGF-β mediated by miR-29c was at the posttranslational level. Meanwhile, we found that 3'-UTR of TGF-β was the direct target of miR-29c confirmed by dual-luciferase assay. In conclusion, our study revealed that miR-29c could alleviate hyperglycemic-induced inflammation and ROS production via targeting TGF-β in cardiomyocytes, which provides a potential target for the treatment of DCM.
Keywords: Diabetes; Diabetic cardiomyopathy; Inflammation; TGF-β; miR-29c.
© 2023. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.