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Activation of Fas inhibits heat-induced activation of HSF1 and up-regulation of hsp70

GEORG SCHETT^*1, CARL-WALTER STEINER^*, MARION GRÖGER, STEFAN WINKLER, WINFRIED GRANINGER^*, JOSEF SMOLEN^*, QINGBO XU^§ and GÜNTER STEINER^||

^* Division of Rheumatology, Department of Internal Medicine III,
Department of Immunodermatology,
Division of Infectiology, Department of Internal Medicine I, University of Vienna;
^§ Institute for Biomedical Aging Research, Austrian Academy of Sciences, Innsbruck; and
^|| Ludwig Boltzmann-Institute for Rheumatology and Balneology, Vienna, Austria

¹Correspondence: Division of Rheumatology, Department of Internal Medicine III, University of Vienna, Währinger Gürtel 18–20, A-1090 Vienna, Austria.

Activation of heat shock factor (HSF) 1-DNA binding and inducible heat shock protein (hsp) 70 (also called hsp72) expression enables cells to resist various forms of stress and survive. Fas, a membrane-bound protein, is a central proapoptotic factor; its activation leads to a cascade of events, resulting in programmed cell death. These two mechanisms with contradictory functions, promoting either cell survival or death, were examined for their potential to inhibit each other's activation. Induction of FAS-mediated signaling was followed by a rapid decrease in HSF1-DNA binding and inducible hsp70 expression. Inhibition of HSF1-DNA binding was demonstrated to be based on absent hyperphosphorylation of HSF1 during FAS signaling. These effects of FAS activation on the HSF1/hsp70 stress response were blocked by ICE (caspase 1) inhibitors, suggesting an ICE-mediated process. Furthermore, inhibition of HSF1/hsp70 was accompanied by an increase in apoptosis rates from 20% to 50% in response to heat stress. When analyzing the effects of HSF1/hsp70 activation on Fas-mediated apoptosis, protection from apoptosis was seen in cells with induced hsp70 protein levels, but not in cells that were just induced for HSF1-DNA binding. Thus, we conclude that inhibition of HSF1/hsp70 stress response during Fas-mediated apoptosis and vice versa may facilitate a cell to pass a previously chosen pathway, stress resistance or apoptosis, without the influence of inhibitory signals.—Schett, G., Steiner, C.-W., Gröger, M., Winkler, S., Graninger, W., Smolen, J., Xu, Q., Steiner, G. Activation of Fas inhibits heat-induced activation of HSF1 and up-regulation of hsp70.

Key Words: Fas activation • antibody • heat shock element • apoptosis • hsp

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