| Abstract: | The role of the cytoskeleton in regulation of purinergic agonist- and endoplasmic Ca(2+)-ATPase inhibitors-induced Ca2+ signals in rat peritoneal macrophages was investigated. It has been shown that in cells pretreated with agents that disrupt microtubules (vinblastine, colchicine, colcemid) or actin microfilaments (cytochalasins, phalloidin), the ability of thapsigargin or cyclopiazonic acid to empty Ca2+ stores and activate store-dependent Ca2+ influx was significantly attenuated. On the contrary, microfilaments and microtubule disrupters did not affect ATP- or UTP-induced Ca2+ mobilization, indicating that release of Ca2+ from intracellular stores through the inositol phosphate pathway was intact. The results suggested that an intact cytoskeleton is required for capacitative Ca2+ entry but not for agonist-induced Ca2+ mobilization. |
