Modulation of dexamethasone-induced thymocyte apoptosis by heat-shock protein 90-binding agents

The Bulletin of Tokyo Dental College
Kazumasa OhtaHarutoshi Kizaki

Abstract

Heat-shock protein 90 (HSP90) is known to affect a variety of cellular activities. The present study showed that the HSP90-binding agents, geldanamycin, herbimycin A and radicicol, inhibited the murine thymocyte apoptosis induced by dexamethasone and was accompanied by the inhibition of the reduction of the mitochondrial transmembrane potential (delta psi m). HSP90-binding agents did not inhibit etoposide-induced apoptosis. The inhibition of dexamethasone-induced apoptosis was in part due to the interference of HSP90 with the glucocorticoid receptor, resulting in the inhibition of nuclear translocation of the receptor. The expression of inositol 1,4,5-triphosphate receptors, which were shown to be involved in dexamethasone-induced apoptosis, did not participate in the inhibition of apoptosis.

References

Feb 1, 1979·Journal of Cellular Physiology·J M HarmonE B Thompson
Jan 1, 1985·Annual Review of Genetics·K R Yamamoto
Jul 15, 1994·Biochemical and Biophysical Research Communications·E LeeK Kariya
Jan 1, 1993·Microbiology and Immunology·H Kizaki, T Tadakuma
Sep 1, 1996·The Journal of Experimental Medicine·P MarchettiG Kroemer
Jan 14, 2000·Journal of Clinical Immunology·Y Yang, J D Ashwell
Mar 8, 2000·The Journal of Immunology : Official Journal of the American Association of Immunologists·P D YorginL Whitesell
Jun 3, 2000·Annual Review of Immunology·J D AshwellM S Vacchio
Dec 19, 2000·Biochemical and Biophysical Research Communications·S L Planey, G Litwack
May 2, 2002·Cell·Astar Winoto, Dan R Littman
Mar 22, 2003·Science·Guy WerlenEd Palmer
May 6, 2003·Biochemical and Biophysical Research Communications·Guido Kroemer
May 9, 2003·The Journal of Biological Chemistry·Zhengqi WangClark W Distelhorst
Oct 8, 2003·Current Cancer Drug Targets·Yoshimasa Uehara

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