Literature DB >> 27390088

ErbB2 is required for cardiomyocyte proliferation in murine neonatal hearts.

Hong Ma1, Chaoying Yin1, Yingao Zhang1, Li Qian1, Jiandong Liu2.   

Abstract

It has been long recognized that the mammalian heart loses its proliferative capacity soon after birth, yet, the molecular basis of this loss of cardiac proliferation postnatally is largely unknown. In this study, we found that cardiac ErbB2, a member of the epidermal growth factor receptor family, exhibits a rapid and dramatic decline in expression at the neonatal stage. We further demonstrate that conditional ablation of ErbB2 in the ventricular myocardium results in upregulation of negative cell cycle regulators and a significant reduction in cardiomyocyte proliferation during the narrow neonatal proliferative time window. Together, our data reveal a positive correlation between the expression levels of ErbB2 with neonatal cardiomyocyte proliferation and suggest that reduction in cardiac ErbB2 expression may contribute to the loss of postnatal cardiomyocyte proliferative capacity.
Copyright © 2016 Elsevier B.V. All rights reserved.

Entities:  

Keywords:  Cardiomyocyte; ErbB2; Neonatal; Proliferation

Mesh:

Substances:

Year:  2016        PMID: 27390088      PMCID: PMC5344651          DOI: 10.1016/j.gene.2016.07.006

Source DB:  PubMed          Journal:  Gene        ISSN: 0378-1119            Impact factor:   3.688


  26 in total

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Authors:  K F Lee; H Simon; H Chen; B Bates; M C Hung; C Hauser
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Review 8.  Advances in understanding tissue regenerative capacity and mechanisms in animals.

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Review 5.  Neuregulins: protective and reparative growth factors in multiple forms of cardiovascular disease.

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6.  Nrg1β Released in Remote Ischemic Preconditioning Improves Myocardial Perfusion and Decreases Ischemia/Reperfusion Injury via ErbB2-Mediated Rescue of Endothelial Nitric Oxide Synthase and Abrogation of Trx2 Autophagy.

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