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Articles in PresS, published online ahead of print October 2, 2002
Am J Physiol Gastrointest Liver Physiol, 10.1152/ajpgi.00076.2002
Submitted on February 20, 2002
Accepted on September 30, 2002
1 Klinik and Poliklinik fur Anasthesiologie und operative Intensivmedizin, Universitatsklinikum Munster, Munster, Germany; Department of Critical Care Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA
2 Department of Critical Care Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA
3 Department of Surgery, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA; Department of Surgery, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA
4 Department of Surgery, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA; Department of Critical Care Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA
5 Department of Critical Care Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA; Department of Pathology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA
* To whom correspondence should be addressed. E-mail: finkmp{at}ccm.upmc.edu.
Cellular adaptation to hypoxia depends in part upon the transcription factor, hypoxia-inducible factor-1 (HIF-1). Normoxic cells exposed to an inflammatory milieu often manifest phenotypic changes, such as increased glycolysis, that are reminiscent of those observed in hypoxic cells. Accordingly, we investigated the effects of cytomix -a mixture containing IFN-
, TNF, and IL-1ß -on the expression of HIF-1-dependent proteins under normoxic and hypoxic conditions. Incubation of IEC-6 cells under 1% O2 increased HIF-1 DNA binding and expression
of aldolase A, enolase-1 and VEGF mRNA. Incubation of normoxic cells with cytomix for 48 h also markedly increased HIF-1 DNA binding and expression of mRNAs for these proteins. Incubation of hypoxic cells with cytomix did not inhibit HIF-1 DNA binding or upregulation of
HIF-1 dependent genes in response to hypoxia. Neither cytomix nor hypoxia increased steadystate levels of HIF-1
mRNA. Incubation of IEC-6 cells with cytomix induced NO. biosynthesis, which was blocked if the cultures contained L-NIL. Treatment with L-NIL,
however, failed to significantly alter aldolase A, enolase-1 and VEGF mRNA levels in normoxic cytomix-treated cells. Pro-inflammatory cytokines activate the HIF-1 pathway and increase expression of glycolytic genes in nontransformed rat intestinal epithelial cells, largely through an
NO.-independent mechanism.
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