Two pathways for store-mediated calcium entry differentially dependent on the actin cytoskeleton in human platelets

Juan A Rosado, José J López, Alan G S Harper, Matthew T Harper, Pedro C Redondo, José A Pariente, Stewart O Sage, Ginés M Salido

Research output: Contribution to journalArticle (Academic Journal)peer-review

78 Citations (Scopus)


A major pathway for stimulated Ca(2+) entry in non-excitable cells is activated following depletion of intracellular Ca(2+) 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 Ca(2+) entry (SMCE) in several cell types. Here we identify two mechanisms for SMCE in human platelets activated by depletion of two independent Ca(2+) pools, which are differentially modulated by the actin cytoskeleton. Ca(2+) 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 Ca(2+) 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.
Original languageEnglish
Pages (from-to)29231-5
Number of pages5
JournalJournal of Biological Chemistry
Issue number28
Publication statusPublished - 9 Jul 2004


  • Animals
  • ras Proteins
  • Calcium
  • Antineoplastic Agents
  • Thiazoles
  • Humans
  • Biological Transport
  • Enzyme Inhibitors
  • Cytochalasin D
  • Bicyclo Compounds, Heterocyclic
  • Cytoskeleton
  • Blood Platelets
  • Peptides, Cyclic
  • Hydroquinones
  • Calcium-Transporting ATPases
  • Actins
  • Depsipeptides
  • Thiazolidines
  • Signal Transduction
  • Nucleic Acid Synthesis Inhibitors

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