Dehydroepiandrosterone improves murine osteoblast growth and bone tissue morphometry via mitogen-activated protein kinase signaling pathway independent of either androgen receptor or estrogen receptor

作者：Wang, Ling; Wang, Yu-Dong; Wang, Wen-Jun; Zhu, Ying; Li, Da-Jin^*

来源：Journal of Molecular Endocrinology, 2007, 38(3-4): 467-479.

DOI：10.1677/jme.1.02173

• AGE-RELATED REDUCTIONS
• NITRIC-OXIDE SYNTHASE
• T-CELLS
• NONGENOMIC MECHANISMS
• RETROVIRUS INFECTION
• POSTMENOPAUSAL WOMEN
• SEX STEROIDS
• VITAMIN-E
• FACTOR-I
• MICE

Dehydroepiandrosterone (DHEA) may be a promising agent for postmenopausal osteoporosis (PMO), but its mechanism to modulate osteoblasts (OBs) is yet to be explained. To elucidate the effects of DHEA treatment on the ovariectomized (OVX) mice and its mechanisms, we evaluated the morphology of mice bone tissue and expression of proliferating cell nuclear antigen (PCNA) in the vertebrae-derived OB after having treated the OVX animals with DHEA. The results showed that DHEA administration increased the expression of PCNA in OB and changed the bone tissue morphometry of the PMO model. To further investigate this mechanism, the OB was isolated from neonatal mice calvariae by the enzyme-digested assay, exposed to DHEA, and then analyzed for ultrastructure, DNA content, early apoptotic cells, and phosphorylation of extracellular signal-regulated kinase 1/2. It was found that DHEA promoted proliferation and inhibited apoptosis of OB significantly, via mitogen-activated protein kinase signaling pathway independent of either androgen receptor or estrogen receptor, suggesting that it may exert roles via a DHEA-specific receptor directly, not by way of conversion to androgens or estrogens.

• 出版日期2007-3
• 单位复旦大学; 海南医学院