Key L L, Weichselbaum R R, Carnes D L
Department of Pediatrics, Bowman Gray School of Medicine, Wake Forest University, Winston-Salem, NC 27103.
Bone Miner. 1988 Jan;3(3):201-9.
Calcitriol exposure stimulated a human osteosarcoma cell line, U2-OS, to produce a factor(s) which stimulated bone degradation in human monocyte cultures and osteoclastic bone resorption in fetal rat long bone cultures. The factor(s) was elicited by as little as 10(-10) M calcitriol. The factor is effective in stimulating peripheral blood monocytes to degrade bone, suggesting a direct effect on cellular bone breakdown. The fetal long bone assays suggest that the osteoblast-like cells produce a factor(s) which stimulates osteoclasts. This is confirmed by the fact that human calcitonin added to the long bone cultures blocks the stimulation. The effect of PTH appears to be through the production of factors which stimulate osteoblasts. The present study suggests that a similar factor(s) may be responsible for the effect of calcitriol on bone resorption.
骨化三醇刺激人骨肉瘤细胞系U2-OS产生一种因子,该因子可刺激人单核细胞培养物中的骨降解以及胎鼠长骨培养物中的破骨细胞骨吸收。该因子在低至10^(-10)M的骨化三醇作用下即可产生。该因子能有效刺激外周血单核细胞降解骨,提示其对细胞性骨破坏有直接作用。胎鼠长骨试验表明,成骨样细胞产生一种刺激破骨细胞的因子。添加到长骨培养物中的人降钙素可阻断这种刺激,这一事实证实了这一点。甲状旁腺激素的作用似乎是通过产生刺激成骨细胞的因子来实现的。本研究表明,类似的因子可能是骨化三醇对骨吸收产生作用的原因。