Kinoshita Y, Fukase M, Yamatani T, Chiba T, Nakai M, Tsutsumi M, Fujita T
Biochem Biophys Res Commun. 1987 Apr 29;144(2):741-8. doi: 10.1016/s0006-291x(87)80027-x.
The present study investigated the possible involvement of phosphatidylinositol breakdown and Ca2+-calmodulin complex in the calcitonin-induced stimulation of phosphate transport in LLC-PK1 cells. This cell line with calcitonin receptors possesses Na+-dependent phosphate transport and has been employed as a model for studying the mechanism of renal tubular phosphate transport. (Asu1,7) eel calcitonin stimulated the phosphate transport in LLC-PK1 cells in a dose-dependent fashion with accompanying increase of inositol triphosphate (IP3) production. When the cells were preincubated with the potent calmodulin antagonist, w-7 or w-13, the stimulatory effect of calcitonin on phosphate transport was significantly inhibited. These findings indicate that Ca2+-calmodulin complex formed by increased cytosolic Ca2+, which is mobilized from intracellular pools by IP3, may be involved in the signal transduction of calcitonin in these cells.
本研究调查了磷脂酰肌醇分解和Ca2+-钙调蛋白复合物在降钙素诱导的LLC-PK1细胞磷酸盐转运刺激中的可能作用。这种具有降钙素受体的细胞系具有钠依赖性磷酸盐转运，已被用作研究肾小管磷酸盐转运机制的模型。（Asu1,7）鳗鱼降钙素以剂量依赖性方式刺激LLC-PK1细胞中的磷酸盐转运，并伴随肌醇三磷酸（IP3）生成增加。当细胞与强效钙调蛋白拮抗剂w-7或w-13预孵育时，降钙素对磷酸盐转运的刺激作用被显著抑制。这些发现表明，由IP3从细胞内池动员的胞质Ca2+增加所形成的Ca2+-钙调蛋白复合物可能参与了这些细胞中降钙素的信号转导。
