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

Developmental cell | Oct 15, 2008

http://www.ncbi.nlm.nih.gov/pubmed/18854137

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.

Pubmed ID: 18854137 RIS Download

Mesh terms: Animals | Embryo, Mammalian | Female | Fetal Heart | Genes, Reporter | Green Fluorescent Proteins | Heart | Heterozygote | Homeostasis | Lyases | Male | Mice | Mice, Knockout | Models, Cardiovascular | Mosaicism | Myocardium | Myocytes, Cardiac | Organogenesis | Pregnancy | Transgenes | X Chromosome Inactivation | beta-Galactosidase

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Mouse Genome Informatics (Data, Gene Annotation)

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