A major pathway for stimulated Ca2+ entry in non-excitable cells is activated following depletion of intra-cellular Ca2+ stores. Secretion-like coupling between elements in the plasma membrane (PM) and Ca 2+ stores has been proposed as the most likely mechanism to activate this store-mediated Ca2+ entry (SMCE) in several cell types. Here we identify two mechanisms for SMCE in human platelets activated by depletion of two independent Ca2+ pools, which are differentially modulated by the actin cytoskeleton. Ca2+ entry induced by depletion of a 2,5-di-(tert-butyl)-1,4-hydroquinone (TBHQ)-sensitive pool is increased by disassembly of the actin cytoskeleton and that induced by a TBHQ-insensitive pool is reduced. Stabilization of the actin cytoskeleton prevented Ca 2+ entry by both mechanisms. We propose that the membrane-associated actin network prevents constitutive Ca2+ entry via both pathways. Reorganization of the actin cytoskeleton permits the activation of Ca 2+ entry via both mechanisms, but only SMCE activated by the TBHQ-insensitive pool requires new actin polymerization, which may support membrane trafficking toward the PM.
CITATION STYLE
Rosado, J. A., López, J. J., Harper, A. G. S., Harper, M. T., Redondo, P. C., Pariente, J. A., … Salido, G. M. (2004). Two pathways for store-mediated calcium entry differentially dependent on the actin cytoskeleton in human platelets. Journal of Biological Chemistry, 279(28), 29231–29235. https://doi.org/10.1074/jbc.M403509200
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