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pubmed-article:10913374pubmed:abstractTextHsp70 is induced by hypoxia in most mammalian cell types and contributes to their ability to survive hypoxic episodes. However, little is known about Hsp70 expression in the hypoxia-tolerant endothelial cells (ECs). We investigated the effect of hypoxia on Hsp70 in human microvascular endothelial HMEC-1 cells. Reduction of pO(2) to 2.5% of normal for 20 h stimulated lactate production and the activity of glycolytic enzymes. This metabolic adaptation to hypoxia was accompanied by a remarkable reduction of Hsp70 on the protein level and on the mRNA level. Approximately 12 h after the hypoxic period Hsp70 expression reached pre-hypoxia levels again. Since ECs are adapted to the low oxygen tension of the vasculature they are confronted with a supraphysiological oxygen level during in vitro culture. We suppose that the high Hsp70 under these conditions reflects a stress response which disappears at the more physiological reduced oxygen tension during hypoxia.lld:pubmed
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pubmed-article:10913374pubmed:copyrightInfoCopyright 2000 Academic Press.lld:pubmed
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pubmed-article:10913374pubmed:pagination542-7lld:pubmed
pubmed-article:10913374pubmed:dateRevised2006-11-15lld:pubmed
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pubmed-article:10913374pubmed:articleTitleEndothelial cells downregulate expression of the 70 kDa heat shock protein during hypoxia.lld:pubmed
pubmed-article:10913374pubmed:affiliationSurgical Research Laboratories, University of Vienna, Vienna, A-1090, Austria. rudolf.oehler@akh-wien.ac.atlld:pubmed
pubmed-article:10913374pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:10913374pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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