Sabała Pawelz, Targos Berenika, Caravelli Antonella, Czajkowski Rafał, Lim Dmitri, Gragnaniello Gianni, Santella Luigia, Barańska Jolanta
Laboratory of Signal Transduction, Department of Molecular and Cellular Neurobiology, Nencki Institute of Experimental Biology, Polish Academy of Sciences, 3 Pasteur Str., Warsaw, Poland.
Biochem Biophys Res Commun. 2002 Aug 16;296(2):484-91. doi: 10.1016/s0006-291x(02)00893-8.
The effects of actin cytoskeleton disruption by cytochalasin D and latrunculin A on Ca2+ signals evoked by ADP, UTP or thapsigargin were investigated in glioma C6 cells. Despite the profound alterations of the actin cytoskeleton architecture and cell morphology, ADP and UTP still produced cytosolic calcium elevation in this cell line. However, calcium mobilization from internal stores and Ca2+ influx through store-operated Ca2+ channels induced by ADP and UTP were strongly reduced. Cytochalasin D and latrunculin A also diminished extracellular Ca2+ influx in unstimulated glioma C6 cells previously incubated in Ca2+ free buffer. In contrast, the disruption of the actin cytoskeleton had no effect on thapsigargin-induced Ca2+ influx in this cell line. Both agonist- and thapsigargin-generated Ca2+ entry was significantly decreased by the blocker of store-operated Ca2+ channels, 2-aminoethoxydiphenylborate. The data reveal that two agonists and thapsigargin activate store-operated Ca2+ channels but the mechanism of activation seems to be different. While the agonists evoke a store-mediated Ca2+ entry that is dependent on the actin cytoskeleton, thapsigargin apparently activates an additional mechanism, which is independent of the disruption of the cytoskeleton.
在神经胶质瘤C6细胞中，研究了用细胞松弛素D和拉春库林A破坏肌动蛋白细胞骨架对由ADP、UTP或毒胡萝卜素诱发的Ca2+信号的影响。尽管肌动蛋白细胞骨架结构和细胞形态发生了深刻改变，但ADP和UTP仍能使该细胞系的胞质钙升高。然而，由ADP和UTP诱导的从内部储存库动员钙以及通过储存操纵性Ca2+通道的Ca2+内流被强烈降低。细胞松弛素D和拉春库林A也减少了先前在无钙缓冲液中孵育的未受刺激的神经胶质瘤C6细胞的细胞外Ca2+内流。相反，肌动蛋白细胞骨架的破坏对该细胞系中毒胡萝卜素诱导的Ca2+内流没有影响。储存操纵性Ca2+通道阻滞剂2-氨基乙氧基二苯基硼酸能显著降低激动剂和毒胡萝卜素引起的Ca2+内流。数据表明，两种激动剂和毒胡萝卜素都能激活储存操纵性Ca2+通道，但激活机制似乎不同。激动剂诱发依赖于肌动蛋白细胞骨架的储存介导的Ca2+内流，而毒胡萝卜素显然激活了一种额外的机制，该机制与细胞骨架的破坏无关。
