Developmental response to hypoxia

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Abstract
Molecular mechanisms underlying fetal growth restriction due to placental insufficiency and in utero hypoxia are not well understood. In the current study, time-dependent (3 h-11 days) changes in fetal tissue gene expression in a rat model of in utero hypoxia compared with normoxic controls were inves- tigated as an initial approach to understand molecular events underlying fetal development in response to hypoxia. Under hypoxic conditions, litter size was reduced and IGFBP-1 was up-regulated in maternal serum and in fetal liver and heart. Tissue-specific, distinct regulatory patterns of gene expression were observed under acute vs. chronic hypoxic conditions. Induction of glycolytic enzymes was an early event in response to hypoxia during organ development; consis- tently, tissue-specific induction of calcium homeostasis- related genes and suppression of growth-related genes were observed, suggesting mechanisms underlying hy- poxia-related fetal growth restriction. Furthermore, in- duction of inflammation-related genes in placentas exposed to long-term hypoxia (11 days) suggests a mechanism for placental dysfunction and impaired pregnancy outcome accompanying in utero hypoxia.— Huang, S.-T. J., Vo, K. C. T., Lyell, D. J., Faessen, G. H., Tulac, S., Tibshirani, R., Giaccia, A. J., Giudice, L. C. Developmental response to hypoxia. FASEB J. 18, 1348 -1365 (2004)
Funding Information
  • National Institutes of Health (NIH 5 R01 HD36732)