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Article |

Heat Shock Induces IκB-α 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. doi:10.1001/archsurg.1997.01430360029005.
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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 α 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 α 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 α 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


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