Finkelman R D, Mohan S, Linkhart T A, Abraham S M, Boussy J P, Baylink D J
Department of Periodontics, Loma Linda University, CA.
Bone Miner. 1992 Feb;16(2):89-100. doi: 10.1016/0169-6009(92)90879-i.
Injections of parathyroid hormone (PTH) result in increased bone formation in several species. Work in our laboratory and others has shown a stimulation of bone cell proliferation and growth factor production by PTH. Our purpose was to study the effects of PTH on a human bone cell line using TE-85 human osteosarcoma cells as a model. After 24 h treatment, PTH caused an increase in cell proliferation as measured by cell counts and [3H]-thymidine incorporation. Proliferation was not inhibited by an anti-transforming growth factor beta (TGF beta) antibody which could abolish stimulation by exogenous TGF beta. PTH did not stimulate cAMP production, alkaline phosphatase activity or production of insulin-like growth factors I or II (IGF-I or IGF-II) in TE-85 cells. Although basal TE-85 proliferation was slowed by incubation with the calcium channel blocking agent verapamil, PTH still caused an increase in growth rate. We conclude that PTH directly stimulates TE-85 proliferation via a mechanism not involving increased adenylate cyclase activity or increased secretion of IGF-I, IGF-II or TGF beta and may stimulate bone formation in vivo by activating some other mitogenic signal to increase bone cell proliferation.
注射甲状旁腺激素（PTH）会使多种物种的骨形成增加。我们实验室及其他机构的研究表明，PTH可刺激骨细胞增殖和生长因子生成。我们的目的是以TE-85人骨肉瘤细胞为模型，研究PTH对人骨细胞系的影响。处理24小时后，通过细胞计数和[3H] - 胸腺嘧啶核苷掺入法检测发现，PTH可使细胞增殖增加。增殖并未被抗转化生长因子β（TGFβ）抗体抑制，而该抗体可消除外源性TGFβ的刺激作用。PTH不会刺激TE-85细胞中的cAMP生成、碱性磷酸酶活性或胰岛素样生长因子I或II（IGF-I或IGF-II）的生成。尽管用钙通道阻滞剂维拉帕米孵育会使TE-85细胞的基础增殖减缓，但PTH仍会使生长速率增加。我们得出结论，PTH通过一种不涉及腺苷酸环化酶活性增加或IGF-I、IGF-II或TGFβ分泌增加的机制直接刺激TE-85细胞增殖，并且可能通过激活其他有丝分裂信号来增加骨细胞增殖，从而在体内刺激骨形成。
