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Compensatory growth of healthy cardiac cells in the presence of diseased cells restores tissue homeostasis during heart development

Official URL:https://doi.org/10.1016/j.devcel.2008.09.005
PubMed:View item in PubMed
Creators Name:Drenckhahn, J.D. and Schwarz, Q.P. and Gray, S. and Laskowski, A. and Kiriazis, H. and Ming, Z. and Harvey, R.P. and Du, X.J. and Thorburn, D.R. and Cox, T.C.
Journal Title:Developmental Cell
Journal Abbreviation:Dev Cell
Volume:15
Number:4
Page Range:521-533
Date:14 October 2008
Keywords:Devbio, Cellcycle, Humdisease, Animals, Mice
Abstract:Energy generation by mitochondrial respiration is an absolute requirement for cardiac function. Here, we used a heart-specific conditional knockout approach to inactivate the X-linked gene encoding Holocytochrome c synthase (Hccs), an enzyme responsible for activation of respiratory cytochromes c and c1. Heterozygous knockout female mice were thus mosaic for Hccs function due to random X chromosome inactivation. In contrast to midgestational lethality of Hccs knockout males, heterozygous females appeared normal after birth. Analyses of heterozygous embryos revealed the expected 50:50 ratio of Hccs deficient to normal cardiac cells at midgestation; however, diseased tissue contributed progressively less over time and by birth represented only 10% of cardiac tissue volume. This change is accounted for by increased proliferation of remaining healthy cardiac cells resulting in a fully functional heart. These data reveal an impressive regenerative capacity of the fetal heart that can compensate for an effective loss of 50% of cardiac tissue.
ISSN:1534-5807
Publisher:Cell Press (U.S.A.)
Item Type:Article

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