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Updated: Mar 18, 2026
Myocardial Infarction in Neonatal Mice, A Model of Cardiac Regeneration
Published on: May 24, 2016
ErbB2 is required for cardiomyocyte proliferation in murine neonatal hearts
Hong Ma1, Chaoying Yin1, Yingao Zhang1
1Department of Pathology and Laboratory Medicine, McAllister Heart Institute, University of North Carolina, Chapel Hill, NC 27599, USA.
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.
Insights
The mammalian heart loses its ability to grow after birth. This study shows that a decrease in ErbB2 (a growth factor receptor) expression is linked to reduced cardiomyocyte proliferation, potentially explaining this loss.
Area of Science:
- Cardiovascular Biology
- Molecular Cardiology
- Developmental Biology
Background:
- Mammalian heart loses proliferative capacity postnatally.
- Molecular mechanisms underlying this loss are largely unknown.
Purpose of the Study:
- Investigate the role of ErbB2 in neonatal cardiomyocyte proliferation.
- Determine the molecular basis for the loss of cardiac proliferative capacity after birth.
Main Methods:
- Assessed ErbB2 expression in neonatal heart.
- Utilized conditional ablation of ErbB2 in ventricular myocardium.
- Analyzed cell cycle regulators and cardiomyocyte proliferation.
Main Results:
- Cardiac ErbB2 expression declines rapidly at the neonatal stage.
- Conditional ablation of ErbB2 upregulated negative cell cycle regulators.
- ErbB2 ablation significantly reduced cardiomyocyte proliferation during the neonatal window.
Conclusions:
- Cardiac ErbB2 expression positively correlates with neonatal cardiomyocyte proliferation.
- Reduced cardiac ErbB2 expression may contribute to the loss of postnatal cardiomyocyte proliferative capacity.
