PARP1 interacts with STAT3 and retains active phosphorylated-STAT3 in nucleus during pathological myocardial hypertrophy.

The activation of signal transducer and activator of transcription 3 positively regulates myocardial hypertrophy, and its transcriptional activity is finely conditioned by diverse extracellular growth factors and cytokines. Here, we introduce novel evidence that poly(ADP-ribose) polymerase 1 interacts with and promotes its activation in cardiomyocytes and rat heart tissues. activity and phosphorylated duanyu18133 were augmented by hypertrophic stimuli both in vitro and in vivo. Infection of Pduanyu371 adenovirus induced cardiomyocyte hypertrophy, which could be prevented by duanyu18133 knockdown or inhibition. Additionally, Pduanyu371 enhanced duanyu18133 phosphorylation level, nuclear accumulation and transcriptional activity. Mechanistically, Pduanyu371 interacts with duanyu18133 and retains active in nucleus. In conclusion, our findings provide the first evidence that Pduanyu371 exacerbates cardiac hypertrophy by stabilizing active which suggests that multi-target therapeutic strategies counteracting Pduanyu371 activity and duanyu18133 activation would be potential for treating cardiovascular diseases.

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