PMID: 11317684Apr 25, 2001Paper

Hypoxia-inducible factor-1 activation and cyclo-oxygenase-2 induction are early reperfusion-independent inflammatory events in hemorrhagic shock

Archives of Orthopaedic and Trauma Surgery
C HierholzerD J Tweardy

Abstract

Hemorrhagic shock (HS) initiates an inflammatory response that includes increased expression of inducible nitric oxide synthase (iNOS) and production of prostaglandins. Induction of iNOS during the ischemic phase of HS may involve the activation of the hypoxia-inducible factor-1 (HIF-1). Increased expression of cyclooxygenase-2 (COX-2) during HS contributes to prostaglandin production. The aim of this study was to determine whether the ischemic phase of HS results in the activation of HIF-1 and the induction of COX-2. The lungs of rats subjected to HS demonstrated a twofold increase in HIF-1 activation (P < 0.01) and a 7.4-fold increase in expression of COX-2 mRNA (P < 0.01) compared with sham controls. The upregulation of iNOS and COX-2 during ischemia are two important early response genes that promote the inflammatory response and may contribute to organ damage through the rapid and exaggerated production of nitric oxide and prostaglandins.

Citations

Oct 15, 2010·Journal of Virology·Neelam Sharma-WaliaBala Chandran
Aug 7, 2010·American Journal of Physiology. Gastrointestinal and Liver Physiology·Rena FeinmanDa-Zhong Xu
Dec 25, 2010·American Journal of Physiology. Gastrointestinal and Liver Physiology·Kolenkode B KannanRena Feinman
Mar 6, 2003·British Journal of Cancer·M KorbelikH Zeng
Jul 1, 2012·Asia-Pacific Journal of Ophthalmology·Widya ArtiniAung Tin
Aug 4, 2006·American Journal of Physiology. Renal Physiology·Ningjun LiPin-Lan Li
May 11, 2017·Molecular Medicine Reports·Xinwei LiuLiangbi Xiang

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