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Estrogen‐induced resistance to osteoblast apoptosis is associated with increased hsp27 expression
Author(s) -
Cooper Lyndon F.,
Tiffee John C.,
Griffin John P.,
Hamano Hideya,
Guo Zhanying
Publication year - 2000
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/1097-4652(200012)185:3<401::aid-jcp10>3.0.co;2-c
Subject(s) - staurosporine , apoptosis , viability assay , estrogen , annexin , estrogen receptor , annexin a5 , osteoblast , biology , microbiology and biotechnology , tunel assay , chemistry , kinase , endocrinology , protein kinase a , biochemistry , in vitro , genetics , cancer , breast cancer
Estrogen has been shown to protect osteoblastic cells from apoptosis. Similarly, estrogen treatment preceding heat shock elevates heat shock protein 27 (hsp27) expression and increases thermoresistance in the murine estrogen receptor‐transformed SMER14 osteoblastic cell line. Forced expression of hsp27 expression in other cell lines limits apoptosis. The purpose of this study was to examine the effects of estrogen on staurosporine‐induced apoptosis in the context of hsp27 expression. Cell viability was measured by the MTT assay. Early apoptotic events were examined by fluorescent microscopy by using FITC‐conjugated Annexin V staining. TUNEL labeling was used to compare the number of apoptotic nuclei following staurosporine treatment of estrogen pretreated or untreated cells. Estrogen treatment increased SMER14 cell viability, but not ROS17/2.8 cell viability, in the presence of staurosporine. Estrogen treatment also reduced annexin V staining and DNA fragmentation. Similar treatment increased SMER14 cell hsp27 levels. The concurrent reduction 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. © 2000 Wiley‐Liss, Inc.