Role of ubiquitin E3 ligase TRIM10 in regulating cardiomyocyte hypertrophy

AIM: To explore the role of ubiquitin E3 ligase tripartite motif 10 (TRIM10) in the development of cardiomyocyte hypertrophy. METHODS: Primary cultured neonatal rat cardiomyocytes (NRCMs) were infected with siRNA-TRIM10, siRNA-control, Ad-TRIM10 or Ad-GFP for 24 h respectively, and then stimulated with phenylephrine (PE) for additional 24 h. The protein levels of TRIM10, AKT and ERK1/2 were determined by Western blot. The size of the NRCMs was measured by immunofluorescence staining. The mRNA expression of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) was detected by RT-qPCR. RESULTS: Compared with the control, PE treatment significantly increased the protein expression of TRIM10. Moreover, transfection of NRCMs with siRNA-TRIM10 markedly inhibited cardiomyocyte size, the mRNA expression of ANP and BNP, and the phosphorylation levels of AKT and ERK as compared with siRNA-control after PE treatment. In contrast, overexpression of TRIM10 significantly enhanced PE-induced hypertrophic effect on NRCMs above. CONCLUSION: TRIM10 regulates cardiomyocyte hypertrophy partially through AKT and ERK signaling pathways.