17-ΒETA-ESTRADIOL PREVENTS OXIDATIVE STRESS-INDUCED APOPTOSIS IN OSTEOCYTES BY GSTP1-1 OVEREXPRESSION

Estrogen plays an important role in bone growth and in regulating bone turnover in adult bone. Estrogen deficiency causes bone loss, increased oxidative stress and osteocyte apoptosis. This leads to increased bone turnover and resorption observed in osteoporosis in postmenopausal women. Previously, it has been demonstrated in osteocytes that starvation induced-apoptosis is related to reactive oxygen species (ROS) production, c-Jun N-terminal kinase (JNK) activity and alteration of factors involved in bone remodeling. The aim of this study was to identify molecular mechanism by which 17β-Estradiol (17β-E2) prevents osteocyte apoptosis induced by oxidative stress. The data demonstrate that 17β-E2 is able to prevent osteocyte apoptosis by a non-redox-regulated mechanism involving GSTP1-1 overexpression and JNK activity inhibition. They suggest a possible role of GSTP1-1 in bone repair mechanisms.