STUDIES ON CAPACITATIVE CALCIUM ENTRY IN CELLULAR SIGNAL TRANSDUCTION

在大鼠胶质瘤C6细胞、人白血病Jurkat细胞和培养的大鼠肝细胞中，研究了Ca^<2+>偶联胞内Ca^<2+>池（ICP）进入，称为“容性Ca^<2+>进入”。在C6细胞中，由bombesin和thapsigargin（一种微粒体Ca^<2+>- atp酶抑制剂）诱导的细胞质游离Ca^<2+>浓度（[Ca^<2+>]_i）的持续增加在粉防己碱（一种受体操作的Ca^<2+>通道（ROC）抑制剂）存在下被消除。百日毒（IAP）、磷酚酯、蛋白激酶C （C-激酶）抑制剂、酪氨酸激酶抑制剂和细胞骨架抑制剂预处理均不影响bombesin和TG诱导的[Ca^<2+>] _i。在Jurkat细胞中，至少存在两种icp，它们都是ip_3和溶血磷酸（LPA）敏感的，LPA敏感的icp与“容性Ca^<2+>进入”无关。在培养的肝细胞中，TG不引起Ca^<2+>振荡。钌红抑制血管加压素诱导的Ca^<2+>振荡，但对TG诱导的[Ca^<2+>] _i振荡无抑制作用。我们认为，iap敏感的gtp结合蛋白、c激酶、酪氨酸激酶和细胞骨架不参与“容性Ca^<2+>进入”的激活，“容性Ca^<2+>进入”与Ca^<2+>振荡无关。此外，似乎存在两种icp，其中一种与“容性Ca^<2+>入口”耦合。

Ca^<2+> entry coupled to intracellular Ca^<2+> pool (ICP), which is called "capacitative Ca^<2+> entry", was investigated in rat glioma C6 cells, human leukemia Jurkat cells and cultured rat hepatocytes. In C6 cells, the sustained increase in cytosolic free Ca^<2+> concentration ([Ca^<2+>]_i)induced by bombesin and thapsigargin (TG), a microsomal Ca^<2+>-ATPase inhibitor, was abolished in the presence of tetrandrine, a receptor-operated Ca^<2+> channel (ROC) inhibitor. The pretreatment with pertussis toxin (IAP), phorbol ester, protein kinase C (C-kinase) inhibitor, tyrosine kinase inhibitor or cytoskeleton inhibitor did not affect [Ca^<2+>] _i induced by bombesin and TG.In Jurkat cells, at least two kinds of ICPs, both of which are IP_3-and lysophosphatic acid (LPA)-sensitive, existed and LPA sensitive-ICP did not relate to "capacitative Ca^<2+> entry." In cultured hepatocytes, TG did not cause Ca^<2+> oscillation. Ruthenium red inhibited Ca^<2+> oscillation induced by vasopressin but not [Ca^<2+>] _i induced by TG.We suggest that IAP-sensitive GTP-binding protein, C-kinase, tyrosine kinase and cytoskeleton are not involved in the activation of "capacitative Ca^<2+> entry" and that "capacitativeCa^<2+> entry" does not relate to Ca^<2+> oscillation. Furthermore, there seems to exist two kinds of ICPs, one of which couples to "capacitative Ca^<2+> entry."