Journal
DEVELOPMENTAL CELL
Volume 2, Issue 3, Pages 331-341Publisher
CELL PRESS
DOI: 10.1016/S1534-5807(02)00131-4
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Funding
- NATIONAL CANCER INSTITUTE [P01CA067166, R37CA088480, R01CA088480] Funding Source: NIH RePORTER
- NCI NIH HHS [CA88480, CA67166, CA09302] Funding Source: Medline
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Cellular differentiation involves transcriptional responses to environmental stimuli. Adipocyte differentiation is inhibited under hypoxic conditions, indicating that oxygen (O-2) is an important physiological regulator of adipogenesis. Hypoxia inhibits PPARgamma2 nuclear hormone receptor transcription, and overexpression of PPARgamma2 or C/EBPbeta stimulates adipogenesis under hypoxia. Mouse embryonic fibroblasts deficient in hypoxia-inducible transcription factor 1alpha (HIF-1alpha) are refractory to hypoxia-mediated inhibition of adipogenesis. The HIF-1-regulated gene DEC1/Stra13, a member of the Drosophila hairy/Enhancer of split transcription repressor family, represses PPARgamma2 promoter activation and functions as an effector of hypoxia-mediated inhibition of adipogenesis. These data indicate that an O-2-sensitive signaling mechanism regulates adipogenesis. Thus, agents that regulate HIF-1 activity or O-2 sensing may be used to inhibit adipogenesis and control obesity.
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