作者: G. Gu , T. A. Hentunen , M. Nars , P. L. Härkönen , H. K. Väänänen
DOI: 10.1007/S10495-005-1893-0
关键词:
摘要: Glucocorticoid-induced osteoporosis may be at least in part due to the increased apoptosis of osteocytes. To study role osteocyte glucocorticoid-induced osteoporosis, we isolated primary osteocytes from murine calvaria for analysis effects dexamethasone vitro culture. The cells were identified by morphology, cytochemical staining, immunocytochemical staining and mRNA expression phosphate-regulating gene with homology endopeptidases on X chromosome (PHEX) sclerosteosis/van Buchem disease (SOST). We found that induced a dose-dependent manner. A glucocorticoid receptor antagonist, mifepristone (RU486), suppressed dexamethasone-induced apoptosis, suggesting it was mediated receptor. Immunocytochemical stainings showed receptors are present osteocytes, they translocated nuclei after exposure dexamethasone. Addition estrogen prevented translocation into nuclei. Corresponding antiapoptotic also seen pretreatment picomolar concentration estrogen. pure antiestrogen ICI 182,780 inhibited effect These data suggest play an important apoptosis. Most importantly, has protective {against osteocyte}{ }{apoptosis}. conclude, mechanism which can opposed