Thermotolerance induced at a mild temperature of 40 degrees C protects cells against heat shock-induced apoptosis.

Abstract:

:Apoptosis constitutes a response of organisms to various physiological or pathological stimuli, and to different stresses. The ability of thermotolerance induced at a mild temperature of 40 degrees C to protect against activation of the apoptotic cascade by heat shock was investigated. When Chinese hamster ovary and human adenocarcinoma cervical cells were pretreated at 40 degrees C for 3 h, they were resistant to subsequent lethal heat shock at 43 degrees C. Induction of thermotolerance at 40 degrees C led to increased expression of heat shock proteins 27, 32, 72, and 90. Heat shock induced apoptotic events at the mitochondrial level, involving a decrease in membrane potential, translocation of Bax to mitochondria, and liberation of cytochrome c into the cytosol. These events were diminished in thermotolerant cells. Heat shock (42-45 degrees C) caused activation of initiator caspase-9 and effector caspases-3, -6, and -7, relative to controls at 37 degrees C. Activation of caspases was decreased in thermotolerant cells. Heat shock caused fragmentation of the caspase substrate, inhibitor of caspase-activated DNase. Fragmentation was diminished in thermotolerant cells. Thermotolerance afforded protection against heat shock-induced nuclear chromatin condensation, but not against necrosis.

journal_name

J Cell Physiol

authors

Bettaieb A,Averill-Bates DA

doi

10.1002/jcp.20386

keywords:

subject

Has Abstract

pub_date

2005-10-01 00:00:00

pages

47-57

issue

1

eissn

0021-9541

issn

1097-4652

journal_volume

205

pub_type

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