FSH enhancing the RANKL‐induced Osteoclastogenesis

Abstract

Recent studies argue whether the declined estrogen or the increased follicle stimulating hormone (FSH) levels is responsible for the postmenopausal osteoporosis. Our recent efforts have been devoted to examining the role of FSH in bone resorption. To test the possible effect of FSH, RAW 264.7 cells was treated with 0, 25, 50, 100 ng/ml RANKL, with/without 0, 5, 30, 100 ng/ml FSH. The RANKL‐induced osteoclastogenesis is in a dose‐dependent manner. FSH alone did not induce the formation of osteoclast. However, FSH augments the RANKL‐induced osteoclastogenesis. The differentiation markers of osteoclast are also examined in this study. The TRAP activity could be stained on the multinucleated osteoclast cells. In addition, the mRNA expressions of RANK, TRAP, cathepsin K, osteopontin and MMP 9 in RANKL‐treated RAW 264.7 cells were also examined by PCR analyses. The combination of RANKL and FSH treatment increases these marker mRNA expressions, except MMP 9 mRNA, compared to those of the RANKL alone group. The protein levels of these osteoclast markers related to the dose of FSH are currently undertaken. The results appear to support the observation reported by Sun et al. [Cell 125:247‐60, 2006]. Our data up to now indicate that FSH appears to modulate RANKL‐induced osteoclastogenesis and thus affect bone mass. Supported by NSC 97‐3112‐B‐038‐003 (YHT).