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induction in
primary inflammatory cells by TNF-
Division of Surgical Research, Department of Surgery, Rhode Island Hospital and Brown Medical School, Providence, Rhode Island 02903
The expression of the
hypoxia-responsive transcription factor hypoxia-inducible factor
(HIF)-1 during acute inflammation was investigated in experimental
wounds. HIF-1
mRNA was maximally expressed in wound cells 6 h
after injury. HIF-1 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)-, but not interleukin-1
, increased
the HIF-1 protein content of cells isolated 1 and 5 days after
injury, and also of glycogen-elicited peritoneal cells, but not
HIF-1 mRNA. HIF-1 did not accumulate in TNF--treated HeLa,
NIH/3T3, NR8383, or RAW 264.7 cells. Nitric oxide from
S-nitrosoglutathione did not induce HIF-1 accumulation or
modulate the response to TNF-. TNF- 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.
inflammation; wound; hypoxia-inducible factor 1; tumor necrosis
factor-
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