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与细胞内Ca^2+池（ICP）偶联的Ca^2+内流，即“容量性Ca^2+内流”。在C6细胞中，蛙皮素和毒胡萝卜素（TG）（一种微粒体Ca^2+-ATP酶抑制剂）引起的胞浆游离Ca^2+浓度（[Ca^2+] i）的持续升高，在存在受体操纵性Ca^2+通道（ROC）抑制剂粉防己碱的情况下被消除。用百日咳毒素（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预处理Jurkat细胞，均不影响蛙皮素和TG诱导的[Ca ^2 +] _i。“在培养的肝细胞中，TG不引起Ca^<2+>振荡。钌红可抑制加压素引起的Ca^<2+>振荡，但对TG引起的[Ca^<2+] _i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“电容性Ca ^<2+>内流”的激活，“电容性Ca ^<2+>内流”与Ca^<2+>振荡无关。此外，似乎存在两种ICP，其中一种耦合到“电容性Ca^2+进入”。"

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."