PKCζ interacts with STAT3 and promotes its activation in cardiomyocyte hypertrophy.

This study was aimed to investigate the crosstalk between protein kinase C ζ and signal transducer and activator of transcription 3 in cardiomyocyte hypertrophy. In neonatal rat cardiomyocyte hypertrophic model induced by phenylephrine (PE), the levels of phosphorylated and phosphorylated were significantly increased, suggesting the activation of both duanyu1531ζ and duanyu18133 in cardiomyocyte hypertrophy. Overexpression of duanyu1531ζ by adenovirus infection elevated the expressions of hypertrophic markers atrial natriuretic factor (ANF) and brains natriuretic polypeptide (BNP), as well as the cell surface area; while genetic silencing of duanyu1531ζ inhibited PE-induced cardiomyocyte hypertrophy. An interaction between duanyu1531ζ and duanyu18133 in cardiomyocytes was shown by co-immunoprecipitation experiments. Overexpression of duanyu1531ζ increased the phosphorylated level of duanyu18133 at both Ser727 and Tyr705, promoted the nuclear translocation of and enhanced the expression of duanyu18133 downstream target genes c-fos and angiotensinogen (aGT); whereas duanyu1531ζ knockdown prevented PE-induced duanyu18133 activation, nuclear shuttling and transcriptional activation. In conclusion, duanyu1531ζ interacts with duanyu18133 and promotes its activation in cardiomyocyte hypertrophy. Strategies targeting inhibition of signaling pathway suggest a therapeutic potential for cardiac hypertrophy.

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