Barańska J, Chaban V, Czarny M, Sabała P
Nencki Institute of Experimental Biology, Department of Cellular Biochemistry, Warsaw, Poland.
Cell Calcium. 1995 Mar;17(3):207-15. doi: 10.1016/0143-4160(95)90035-7.
Glioma C6 cells treated with 12-0-tetradecanoyl-phorbol-13-acetate, TPA (10 nM and 100 nM) manifested slow increase in intracellular calcium concentration ([Ca2+]i), dependent upon both Ca2+ release from intracellular stores and Ca2+ entry, and ranging from 50 to 500 nM in different cells. The effect of TPA was abolished by the down-regulation procedure and by protein kinase C inhibitors, such as staurosporine (100 nM), suramin (100 microM), and sphingosine (100 microM), pointing to a role of protein kinase C (PKC) in this process. On the other hand, thapsigargin (100 nM), a selective inhibitor of the endoplasmic reticulum Ca(2+)-ATPase, produced a rapid increase in [Ca2+]i (up to 800 nM). This increase consisted of a transient initial phase followed by sustained elevation in [Ca2+]i, typical of Ca2+ release from intracellular stores and of Ca2+ entry, respectively. However, when the cells were exposed to TPA (100 nM) prior to thapsigargin (100 nM), then thapsigargin produced only a transient rise in [Ca2+]i. We suggest that TPA, a PKC activator, affects thapsigargin-induced Ca2+ entry, probably by PKC-mediated changes in cytoskeleton structures.
用12 - 0 - 十四烷酰佛波醇-13 - 乙酸酯（TPA，10 nM和100 nM）处理的胶质瘤C6细胞表现出细胞内钙浓度（[Ca2+]i）缓慢升高，这依赖于细胞内钙库释放Ca2+和Ca2+内流，且不同细胞中[Ca2+]i升高范围为50至500 nM。TPA的作用可通过下调程序以及蛋白激酶C抑制剂（如星形孢菌素（100 nM）、苏拉明（100 μM）和鞘氨醇（100 μM））消除，这表明蛋白激酶C（PKC）在此过程中起作用。另一方面，毒胡萝卜素（100 nM），一种内质网Ca(2+)-ATP酶的选择性抑制剂，使[Ca2+]i迅速升高（高达800 nM）。这种升高包括一个短暂的初始阶段，随后是[Ca2+]i的持续升高，分别典型地代表细胞内钙库释放Ca2+和Ca2+内流。然而，当细胞在毒胡萝卜素（100 nM）之前先暴露于TPA（100 nM）时，那么毒胡萝卜素仅使[Ca2+]i产生短暂升高。我们认为，PKC激活剂TPA可能通过PKC介导的细胞骨架结构变化影响毒胡萝卜素诱导的Ca2+内流。
