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J Appl Physiol 97: 564-569, 2004. First published April 16, 2004; doi:10.1152/japplphysiol.00194.2004
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Geldanamycin treatment inhibits hemorrhage-induced increases in KLF6 and iNOS expression in unresuscitated mouse organs: role of inducible HSP70

Juliann G. Kiang,1,2,3 Phillip D. Bowman,4 Brian W. Wu,1 Nyasa Hampton,1 Andrew G. Kiang,1 Baiteng Zhao,4 Yuang-Taung Juang,1,2 James L. Atkins,1 and George C. Tsokos1,2

1Division of Military Casualty Research, Walter Reed Army Institute of Research, Silver Spring 20910-7500; Departments of 2Medicine and 3Pharmacology, Uniformed Services University of the Health Sciences, Bethesda, Maryland 20814-4799; and 4United States Army Institute of Surgical Research, San Antonio, Texas 78234-6315

Submitted 25 February 2004 ; accepted in final form 10 April 2004

The aim of this study was to determine whether hemorrhage affects the levels of a variety of stress-related proteins and whether changes can be inhibited by drugs reported to provide protection from ischemia and reperfusion injury. Male Swiss Webster mice were subjected to a 40% hemorrhage without resuscitation. Western blot analysis indicated that c-Jun (an AP-1 protein), Kruppel-like factor 6 (KFL6), and inducible nitric oxide synthase (iNOS) were upregulated sequentially in that order. Pretreatment of mice with geldanamycin (GA) 16 h before hemorrhage effectively inhibited the expression of the proteins KLF6 and iNOS, whereas caffeic acid phenethyl ester did not. GA pretreatment increased inducible heat shock protein (HSP) 70 but not HSP90 in both sham and hemorrhagic tissues. The overexpressed inducible HSP70 formed complexes with KLF6 and iNOS. These results suggest that GA may be therapeutically useful for reducing hemorrhage-induced injury when used as a presurgical treatment or when added to resuscitation fluids.

apoptosis; caffeic acid phenethyl ester; c-Jun; c-Fos; nuclear factor-{kappa}B; hypoxia-inducible factor-1; Kruppel-like factor 6 transcription factor


Address for reprint requests and other correspondence: J. G. Kiang, Dept. of Cellular Injury, Division of Military Casualty Research, Walter Reed Army Institute of Research, Silver Spring, MD 20910-7500 (E-mail: Juliann.Kiang{at}na.amedd.army.mil).




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