Pfeilschifter J, D'Souza S M, Mundy G R
Endocrinology. 1987 Jul;121(1):212-8. doi: 10.1210/endo-121-1-212.
Transforming growth factor-beta (TGF beta), a polypeptide that controls growth and differentiation in many cell types and has recently been found in abundant amounts in bone, was examined for its effects on cells with the osteoblast phenotype using the clonal osteoblastic osteosarcoma cell line ROS 17/2.8. TGF beta increased alkaline phosphatase (AP) activity and the rate of collagen synthesis per cell. Cell proliferation was inhibited, and the morphological appearance of the cells was markedly changed. All effects were observed at concentrations as low as 0.1 ng/ml TGF beta. Increases in AP activity were detectable after 24 h and increased progressively with time. TGF beta increased AP activity under serum-free conditions and during thymidine-induced inhibition of DNA synthesis. The increase in AP activity mediated by TGF beta could be completely inhibited with actinomycin D and cycloheximide. 1,25-Dihydroxyvitamin D3 at 10(-7) M slightly increased AP activity in ROS 17/2.8 cells, but strongly inhibited AP activity when the cells were pretreated with TGF beta. The data suggest that TGF beta stimulates expression of the osteoblastic phenotype in ROS 17/2.8 cells and that TGF beta may be an important regulator of local bone remodeling.
转化生长因子-β（TGFβ）是一种控制多种细胞类型生长和分化的多肽，最近发现其在骨中含量丰富。本研究使用克隆成骨骨肉瘤细胞系ROS 17/2.8，检测了TGFβ对具有成骨细胞表型细胞的影响。TGFβ增加了碱性磷酸酶（AP）活性和每个细胞的胶原蛋白合成速率。细胞增殖受到抑制，细胞的形态外观发生明显变化。所有这些效应在TGFβ浓度低至0.1 ng/ml时即可观察到。24小时后可检测到AP活性增加，并随时间逐渐增加。TGFβ在无血清条件下以及在胸苷诱导的DNA合成抑制期间均增加了AP活性。TGFβ介导的AP活性增加可被放线菌素D和环己酰亚胺完全抑制。10^(-7) M的1,25-二羟基维生素D3在ROS 17/2.8细胞中轻微增加了AP活性，但当细胞用TGFβ预处理时则强烈抑制AP活性。数据表明，TGFβ刺激ROS 17/2.8细胞中成骨细胞表型的表达，并且TGFβ可能是局部骨重塑的重要调节因子。
