Abstract: Objective  To investigate the effect and mechanism of microvesicles (MVs) containing miroRNA21(miR21) from tubular epithelial cells in cardiomyocyte hypertrophy.Methods  Renal tubular epithelial cells were stimulated by transforming growth factor β1 (TGFβ1),  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 qPCR,  and the length and diameter of cardiomyocytes were measured by eyepiece. Bicinchoninic acid(BCA) protein kit and atrial natriuretic peptide(ANP) kit were used to detect the content of cell protein and the level of ANP. MiR21 inhibitor was transfected into recipient cardiomyocytes in advance to observe the effects on the length and diameter,  protein content and ANP level of the cells.Results  TGFβ1 could induce donor renal tubular epithelial cells to produce MVs which were then delivered into cardiomyocytes,  and the diameter,  protein content and ANP level of cardiomyocytes were significantly increased. Meanwhile,  miR21 in MVs could cause recipient cardiomyocyte hypertrophy. And pretransfection of miR21 inhibitors could inhibit MVsinduced cardiomyocyte hypertrophy.Conclusion  The damaged renal tubular epithelial cells can secrete MVs containing miR21 which can induce cardiomyocyte hypertrophy. And this may be involved in the progress of chronic kidney disease complicated with heart failure.

Key words: kidney diseases；microRNA, microvesicles, cardiomyocyte hypertrophy