Capacitative calcium entry is inhibited in vascular endothelial cells by disruption of cytoskeletal microfilaments.
The role of an intact cytoskeleton for store-operated ('capacitative') Ca2+ influx was investigated in single cultured vascular endothelial cells. Capacitative Ca2+ entry was measured as changes of cytoplasmic Ca2+ concentration ([Ca2+]i) induced by depletion of Ca2+ stores with thapsigargin. In cells pretreated with cytochalasin D, an agent that disrupts the microfilament network of the cytoskeleton, as confirmed with FITC-phalloidin staining, capacitative Ca2+ entry was inhibited. Cytochalasin D did not affect basal [Ca2+]i nor ATP-induced increases of [Ca2+]i, indicating that release of Ca2+ from intracellular stores through the inositol-phosphate pathway was intact. These results suggest that microfilaments are an integral part of the mechanism for capacitative Ca2+ entry. The necessity for an intact cytoskeleton favors a conformational coupling model for store-operated Ca2+ influx.
Holda
J R
JR
Department of Physiology, Loyola University Chicago, Maywood, IL 60153, USA.
Blatter
L A
LA
D000255:Adenosine Triphosphate / Q000494:pharmacology; D000818:Animals; D002118:Calcium / Q000378:metabolism*; D002417:Cattle; D002478:Cells, Cultured; D003599:Cytoskeleton / Q000187:drug effects / Q000378:metabolism* / Q000648:ultrastructure; D004730:Endothelium, Vascular / Q000187:drug effects / Q000378:metabolism* / Q000648:ultrastructure; D017136:Ion Transport; D018613:Microscopy, Confocal
D000255:Adenosine Triphosphate; D002118:Calcium