Journal
AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY
Volume 281, Issue 6, Pages C1971-C1977Publisher
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpcell.2001.281.6.C1971
Keywords
inflammation; wound; hypoxia-inducible factor 1; tumor necrosis factor-alpha
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Funding
- NIGMS NIH HHS [GM-42859] Funding Source: Medline
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The expression of the hypoxia-responsive transcription factor hypoxia-inducible factor (HIF)-1 during acute inflammation was investigated in experimental wounds. HIF-1 alpha mRNA was maximally expressed in wound cells 6 h after injury. HIF-1 alpha protein was detectable in wound cells 1 and 5 days after injury. Cells from 1-day-old wounds were not hypoxic, as determined by lack of pimonidazole hydrochloride adduct formation. Tumor necrosis factor (TNF)-alpha, but not interleukin-1 beta, increased the HIF-1a protein content of cells isolated 1 and 5 days after injury, and also of glycogen-elicited peritoneal cells, but not HIF-1 alpha mRNA. HIF-1 alpha did not accumulate in TNF-alpha -treated HeLa, NIH/3T3, NR8383, or RAW 264.7 cells. Nitric oxide from S-nitrosoglutathione did not induce HIF-1 alpha accumulation or modulate the response to TNF-alpha. TNF-alpha did not increase oxygen consumption or result in the production of reactive oxygen intermediates by day 1 wound cells. Vascular endothelial growth factor mRNA in wound cells peaked 24 h after wounding. HIF-1 expression in early wounds may contribute to the regulation of inducible nitric oxide synthase and vascular endothelial growth factor, two HIF-1-responsive genes intimately related to the process of repair.
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