| The Antiresorptive Effects of Vitamin K2 on Osteoblasts and Osteoclasts |
| Vitamin K2의 조골세포 및 파골세포에 대한 효과 |
| 황창선,정호연1,강영순,문인걸,임창훈1,한기옥1,장학철1,윤현구1,한인권1,최태부2 |
| 성균관대학교 의과대학 삼성제일병원 내분비 연구실, 내과1, 건국대학교2 |
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| Abstract |
Background
It is widely recognized that vitamin K2 involved in bone metabolism and has beneficial effects on osteoporosis. Vitamin K2 inhibits bone resorption and osteoclast-like cell formation. However, its exact mechanisms to inhibit osteoclast formation and to accelerate osteoblast activity are not fully understood yet. The purpose of this study was to investigate the precise mechanism of vitamin K2induced inhibitory effect on osteoclast formation in mouse marrow culture.
Methods
We assessed the 1,25(OH)2 D3-induced osteoclast formation in mouse marrow culture with or without vitamin K2 for 7 days. Also, ST2, a mouse marrow-derived stromal cells were treated with vitamin K2 10-9 M~10-5 M containing α-MEM supplemented with 1% FBS for 24 hours, and was examined the expression of OPG and RANKL mRNA using semi-quantitative RT-PCR. Vitamin K2 effect on osteoclast apoptosis was identified using the TUNEL method.
Results
After 7 days of incubation, vitamin K2 dose-dependently inhibited the 1,25(OH)2 D3- induced osteoclast formation. The expression of RANKL mRNA was decreased at 10-6 M and 10-5 M of vitamin K2, but the level of OPG mRNA was not changed. The number of apoptotic osteoclast cells was higher in the presence of 10-5 M of vitamin K2 compared to control (23.6±7.4% vs 10.9±0.8%, p<0.05).
Conclusion
These findings suggest that antiresorptive effect of vitamin K2 on bone remodeling was indirectly mediated by osteoblasts and directly by osteoclasts.
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| Key Words:
Vitamin K2, Osteoblast, Oteoclast, RANKL, Apoptosis |
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