MicroRNA-21-containing microvesicles from tubular epithelial cells promote cardiomyocyte hypertrophy

Background Cardiomyocyte hypertrophy has been reported as one of the important mechanisms for cardiovascular disease (CVD) in patients with chronic kidney disease (CKD). MiroRNA-21(miR-21) was determined to play an important role in myocardial hypertrophy. However, the role of microvesicles (MVs) containing miR-21 in CKD-related cardiomyocyte hypertrophy remains largely unexplored. Methods Renal tubular epithelial cells were stimulated by transforming growth factor (TGF-beta 1), and the conditioned medium was extracted by differential centrifugation. Renal tubular epithelial cells were labeled with Dil-C18 dye and the recipient cardiomyocytes were observed by fluorescence microscope. MiR-21 level in MVs was detected by qRT-PCR, and the length and diameter of cardiomyocytes were measured by microscope. BCA protein kit and ANP kit were used to detect the content of cell protein and the level of ANP. MiR-21 inhibitor was transfected into cardiomyocytes to observe the effect of miR-21 on myocardial hypertrophy. Results TGF-beta 1 could induce donor renal tubular epithelial cells to produce MVs and delivered into cardiomyocytes, followed by the diameter, protein concentration and ANP content of cardiomyocytes significantly increased. Meanwhile, MiR-21 levels were markedly increased in MVs isolated from donor renal tubular epithelial cells and recipient cardiomyocytes. Pre-transfection of miR-21 inhibitors could inhibit MV-induced cardiomyocyte hypertrophy. Conclusion Tubular cells could secrete miR-21 by MVs and deliver it into recipient cardiomyocytes to induce cardiomyocyte hypertrophy. It might shed a new light on the mechanism and treatment of CKD-related cardiac dysfunction.

Automated summary

MiR-21 delivered by microvesicles from renal tubular epithelial cells can induce cardiomyocyte hypertrophy, providing new insights into the mechanism and treatment of CKD-related cardiac dysfunction.