Ljunggren O, Johansson H, Lerner U H, Lindh E, Ljunghall S
Department of Internal Medicine, University Hospital, Uppsala, Sweden.
Biosci Rep. 1992 Jun;12(3):207-14. doi: 10.1007/BF01121790.
The effects of parathyroid hormone (PTH) on cytoplasmic free Ca2+ (Cai2+) and cAMP-formation were investigated in the rat osteosarcoma cell line UMR 106-01. In fura-2 loaded adherent single cells bPTH 1-34 (10 nM - 1 microM) induced a rapid transient increase in Cai2+ in 11% of the studied cells. In fura-2 tracings from UMR 106-01 cells in suspension, bPTH 1-34 (0.1 microM) induced a transient increase in Cai2+ in 20% of the experiments. The transient increase in Cai2+ seen in suspensions of cells was not abolished by addition of EGTA (2.5 mM) prior to challenge with PTH, suggesting that the increase in Cai2+ was derived from intracellular stores. A marked rapid increase in cAMP-formation was observed in all experiments with cells in suspension, also in the experiments where PTH did not affect Cai2+. These data show that PTH causes a release of Ca2+ from intracellular stores in a small percentage of osteosarcoma UMR 106-01 cells, and that PTH is capable of inducing an increase in cAMP-formation without affecting Cai2+ in osteoblasts.
在大鼠骨肉瘤细胞系UMR 106-01中研究了甲状旁腺激素（PTH）对细胞质游离Ca2+（Cai2+）和环磷酸腺苷（cAMP）形成的影响。在负载fura-2的贴壁单细胞中，1-34人重组甲状旁腺激素（bPTH 1-34，10 nM - 1 microM）在11%的研究细胞中诱导Cai2+迅速短暂升高。在悬浮的UMR 106-01细胞的fura-2记录中，1-34人重组甲状旁腺激素（bPTH 1-34，0.1 microM）在20%的实验中诱导Cai2+短暂升高。在用PTH刺激之前加入乙二醇双（2-氨基乙醚）四乙酸（EGTA，2.5 mM）并不能消除在细胞悬浮液中观察到的Cai2+短暂升高，这表明Cai2+的升高源自细胞内储存。在所有悬浮细胞实验中均观察到cAMP形成显著快速增加，在PTH不影响Cai2+的实验中也是如此。这些数据表明，PTH在一小部分骨肉瘤UMR 106-01细胞中引起细胞内储存的Ca2+释放，并且PTH能够在不影响成骨细胞中Cai2+的情况下诱导cAMP形成增加。
