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Highlights: [•] Salvianolic acid B (SalB) protected cardiomyocytes from AngII-induced hypertrophy. [•] SalB’ anti-hypertrophy was partly attributed to its inhibition on PARP-1. [•] SalB prevented the depletion of cellular NAD+ induced by AngII. [•] SalB’s antioxidant effect might contribute to the inhibition of PARP-1. [ABSTRACT FROM AUTHOR]

Highlights: [•] In cardiomyocytes, ET-1 treatment resulted in significant upregulation of COX-2 expression and activity. [•] Both COX-2 inhibitors and COX-2 RNA interference suppressed cardiomyocyte hypertrophy induced by ET-1. [•] Calcineurin/NFATc3 signaling pathway participated in the transcriptional regulation of COX-2 by ET-1. [ABSTRACT FROM AUTHOR]

Highlights: [•] C/EBPβ expression is upregulated in response to hypertrophic stimulation in vitro and in vivo. [•] C/EBPβ knockdown protects cardiomyocytes from hypertrophy. [•] C/EBPβ knockdown reduced the nuclear translocation of p65-NFκB, and diminished NFκB-DNA binding activity. [ABSTRACT FROM AUTHOR]

Abstract: Poly(ADP-ribosyl)ation catalyzed by the poly(ADP-ribose) polymerases (PARPs) is an immediate post-translational modification of proteins with a homopolymeric chain of repeating ADP-ribose units. It is involved in various cellular processes, such as cell survival and death, transcription, DNA repair and cell division. Inhibitors of PARPs have been documented to be useful in different pathological conditions. Recently, activation of PARP-1, the founding member of PARP family, has been revealed to participate in the development and progression of cardiac hypertrophy and heart failure. However, the roles of other PARPs in cardiovascular system remain to be clarified. PARP-2 shares 69% similarity with PARP-1 in catalytic domains, but their functions do not fully overlap. In this study, we show the first evidence that PARP-2 is involved in cardiac hypertrophy. The mRNA and protein levels of PARP-2 were significantly increased in AngII-stimulated rat cardiomyocytes as well as in hearts of rats submitted to pressure overload. PARP-2 knockdown protected cardiomyocytes from hypertrophy, which may be attributed to activation of SIRT1. These findings shed new light on the understanding of PARP-2-related cardiomyopathy, and suggest the potential application of PARP-2 inhibitors in cardiac hypertrophy. [Copyright &y& Elsevier]