TBX3 deficiency accelerates apoptosis in cardiomyoblasts through regulation of P21 expression.

Congenital heart disease (CHD) is the most common birth defect in newborns. There is increasing evidence that apoptosis and remodeling of the cardiomyoblasts are the major pathology of CHD. Previous research found that T-box transcription factor 3 (TBX3) was compulsory for the regulation of proliferation, cell cycle arrest and apoptosis in various cells. Hence, TBX3 might be involved in the treatment of CHD. The primary aim of this study was to study the effects of TBX3 on apoptosis in aged cardiomyoblasts and investigate the latent mechanism. In the present study, we found TBX3 knockdown induced proliferation inhibition, cell cycle arrest and apoptosis accompanied by mitochondrial dysfunction in cardiomyoblasts at passage 10 to 15. Apoptosis-inducing effects of TBX3 silence could be neutralized by silencing P21 using specific siRNA. In addition, the mRNA and protein expression levels of TBX3 in the heart tissues of sporadic type CHD donors were obviously down-regulated. In conclusion, we demonstrated that TBX3 deficiency accelerated apoptosis via directly regulating P21 expression in senescent cardiomyoblasts.
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