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Heat Shock Induces IB- and Prevents Stress-Induced Endothelial Cell Apoptosis

Susan L. DeMeester, MD; Timothy G. Buchman, PhD, MD; Yuyu Qiu; Ammini K. Jacob, MBBS, PhD; Keith Dunnigan, MS; Richard S. Hotchkiss, MD; Irene Karl, PhD; J. Perren Cobb, MD

Arch Surg. 1997;132(12):1283-1288.

Abstract
Objective
To determine whether prior heat shock would attenuate endothelial cell apoptosis and whether any effect of preemptive heat shock is mediated through a nuclear factor kappa B and inhibitor kappa B mechanism.

Design
A randomized, controlled in vitro study.

Setting
A laboratory in a large, academic medical center.

Interventions
Cultured primary porcine endothelial cells were treated with increasing doses of sodium arsenite (40-160 µmol/L), after which the interval until subsequent apoptotic (lipopolysaccharide-arsenite) challenge was varied (4-16 hours). The degree of cell death and apoptosis were determined using neutral red uptake and staining with annexin V and propidium iodide, respectively. Inducible heat shock protein 70 and inhibitor kappa B levels in treated cells were determined by Western blot analysis. Lipopolysaccharide-induced nuclear factor kappa B activity was assessed using an electrophoretic mobility shift assay.

Results
Prior arsenite treatment decreased cell death by apoptosis in a time- and dose-dependent manner. Specifically, a higher sodium arsenite concentration and shorter intervals afforded better protection (P=.01, 160 µmol/L at 4 hours). Protection against apoptosis correlated with increased heat shock protein 70 and inhibitor kappa B levels and decreased nuclear factor kappa B binding activity.

Conclusions
Arsenite, an inducer of the heat shock response, decreased stress-induced endothelial cell apoptosis. The mechanism of this protection may include decreased nuclear factor kappa B activity or increased inducible heat shock protein 70 levels. Heat shock protein 70 may serve as a molecular marker to determine not only the phenotypic state of the cell but also the durability of protection afforded by heat shock. These data support the hypothesis that stress-induced changes in transcription factor activity and protein expression can regulate the induction of apoptosis.

Arch Surg. 1997;132:1283-1288

Author Affiliations
From the Cellular Injury and Adaptation Laboratory and the Departments of Surgery (Drs DeMeester, Buchman, Jacob, and Cobb and Ms Qui), Anesthesia (Drs Buchman and Hotchkiss), and Medicine (Drs Buchman and Karl), and the Division of Biostatistics (Mr Dunnigan), Washington University School of Medicine, St Louis, Mo.

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