Adaptive mechanisms that preserve cardiac function in mice without myoglobin.

Journal Article

Mice lacking myoglobin survive to adulthood and meet the circulatory demands of exercise and pregnancy without cardiac decompensation. In the present study, we show that many myoglobin-deficient embryos die in utero at midgestation with signs of cardiac failure. Fetal mice that survive to gestational day 12.5, however, suffer no subsequent excess mortality. Survival in the absence of myoglobin is associated with increased vascularity and the induction of genes encoding the hypoxia-inducible transcription factors 1alpha and 2, stress proteins such as heat shock protein 27, and vascular endothelial growth factor. These adaptations are evident in late fetal life, persist into adulthood, and are sufficient to maintain normal myocardial oxygen consumption during stressed conditions. These data reveal that myoglobin is necessary to support cardiac function during development, but adaptive responses evoked in some animals can fully compensate for the defect in cellular oxygen transport resulting from the loss of myoglobin.

Full Text

Duke Authors

Cited Authors

  • Meeson, AP; Radford, N; Shelton, JM; Mammen, PP; DiMaio, JM; Hutcheson, K; Kong, Y; Elterman, J; Williams, RS; Garry, DJ

Published Date

  • April 13, 2001

Published In

Volume / Issue

  • 88 / 7

Start / End Page

  • 713 - 720

PubMed ID

  • 11304494

Electronic International Standard Serial Number (EISSN)

  • 1524-4571

Language

  • eng

Conference Location

  • United States