STUDIES ON CAPACITATIVE CALCIUM ENTRY IN CELLULAR SIGNAL TRANSDUCTION

在大鼠脑胶质瘤C6细胞、人白血病Jurkat细胞和培养的大鼠肝细胞中，研究了与细胞内钙池(ICP)偶联的钙离子内流，称为“容量性钙内流”。在C6细胞中，蛙皮素和微粒体钙通道(ROC)阻断剂thapsigargin(TG)引起的胞浆游离钙浓度([Ca^&lt；2&gt；]i)的持续升高可被受体操作的钙通道(ROC)阻断剂粉防己碱所阻断。百日咳毒素(IAP)、佛波酯、蛋白激酶C(C-Kinase)抑制剂、酪氨酸激酶抑制剂或细胞骨架抑制剂不影响蛙皮素和TG诱导的[Ca^&lt；2&gt；]_i。在Jurkat细胞中，至少存在两种对IP_3和溶血磷酸(LPA)敏感的ICPs，LPA敏感的ICP与“容量性钙进入”无关。在培养的肝细胞中，甘油三酯不引起钙振荡。Ru红抑制后叶加压素诱导的钙振荡，但不抑制TG诱导的[Ca^&lt；2&gt；]_i。提示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“容积性钙内流”的激活，“容量性钙内流”与钙内流无关。此外，似乎存在两种ICP，其中一种与“容量性钙条目”相结合。

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."