SIRT1 increases cardiomyocyte binucleation in the heart development

Oncotarget
Alexandra N ShinLubo Zhang

Abstract

SIRT1 regulates cell senescence. We investigated a novel role of SIRT1 in the regulation of cardiomyocyte terminal differentiation in the developing heart. Retinoic acid (RA)-induced binucleation of H9c2 cells was associated with increased SIRT1 expression. Inhibition of SIRT1 activity or expression significantly decreased RA-induced binucleation. SIRT1 expression was minimal in the fetal heart and significantly upregulated in the hearts of postnatal day 7 (P7) rat pups. In contrast, heart-specific miR-133a expression was high in the fetal heart but significantly reduced in P7 pup hearts. The miR-133a promoter contains a canonical HRE element and hypoxia upregulated miR-133a gene expression in the heart. SIRT1 mRNA 3'UTR has miR-133a binding sequences and miR-133a and hypoxia suppressed SIRT1 expression in cardiomyocytes. Of importance, inhibition of SIRT1 significantly reduced binucleated cardiomyocytes in the hearts of P7 pups. Taken together, the present study reveals a novel role of SIRT1 and its regulation by miR-133a in cardiomyocyte terminal differentiation of the developing heart, and suggests a potential therapeutic strategy that may impact cardiac function later in life.

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Citations

Jul 19, 2019·Journal of Muscle Research and Cell Motility·Maicon Landim-VieiraP Bryant Chase
Jan 4, 2021·Cellular and Molecular Life Sciences : CMLS·Sanjeev Kumar SoniRussel J Reiter
Jan 14, 2021·Cellular and Molecular Life Sciences : CMLS·Jie Wang AJunlian Gu
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Methods Mentioned

BETA
FACS
flow cytometry
transfection
PCR
LightShift
electrophoresis

Software Mentioned

Image J
FlowJo
Genomatix

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