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Developmental response to hypoxia

S.-T. JOSEPH HUANG^*, KIM CHI T. VO^*, DEIRDRE J. LYELL^*, GERARDA H. FAESSEN^*, SUZANA TULAC^*, R. TIBSHIRANI, AMATO J. GIACCIA and LINDA C. GIUDICE^*,1

Department of
^* Obstetrics and Gynecology,
Health Research and Policy and
Radiation Oncology, Stanford University Medical Center, California, USA

¹Correspondence: Department of Obstetrics and Gynecology, Stanford University Medical Center, 300 Pasteur Dr., Room HH 333, Stanford, CA 94305-5317, USA. E-mail: giudice{at}stanford.edu

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 investigated 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; consistently, tissue-specific induction of calcium homeostasis-related genes and suppression of growth-related genes were observed, suggesting mechanisms underlying hypoxia-related fetal growth restriction. Furthermore, induction 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.

Key Words: intrauterine growth restriction • fetal growth • hypoxic response

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