Estrogen-induced resistance to osteoblast apoptosis is associated with increased hsp27 expression

Estrogen has been shown to protect osteoblastic cells from apoptosis. Simil arly, estrogen treatment preceding heat shock elevates heat shock protein 2 7 (hsp27) expression and increases thermoresistance in the murine estrogen receptor-transformed SMER14 osteoblastic cell line. Forced expression of hs p27 expression in other cell lines limits apoptosis. The purpose of this st udy was to examine the effects of estrogen on staurosporine-induced apoptos is in the context of hsp27 expression. Cell viability was measured by the M TT assay. Early apoptotic events were examined by fluorescent microscopy by using FITC-conjugated Annexin V staining. TUNEL labeling was used to compa re the number of apoptotic nuclei following staurosporine treatment of estr ogen pretreated or untreated cells. Estrogen treatment increased SMER14 cel l viability, but not ROS1712.8 cell viability, in the presence of staurospo rine. Estrogen treatment also reduced annexin V staining and DNA fragmentat ion. Similar treatment increased SMER14 cell hsp27 levels. The concurrent r eduction in induced apoptosis suggests a possible estrogenic mechanism for increasing and/or maintaining the number of viable osteoblasts in bone. J. Cell. Physiol. 185:401-407, 2000. (C) 2000 Wiley-Liss, Inc.