Role of the actin cytoskeleton in store-mediated calcium entry in glioma C6 cells

Pawel Sabala, Berenika Targos, Antonella Caravelli, Rafal Czajkowski, Dmitri Lim, Gianni Gragnaniello, Luigia Santella, Jolanta Barańska

Research output: Contribution to journalArticlepeer-review

Abstract

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.

Original languageEnglish
Pages (from-to)484-491
Number of pages8
JournalBiochemical and Biophysical Research Communications
Volume296
Issue number2
DOIs
Publication statusPublished - 2002
Externally publishedYes

Keywords

  • ADP
  • Actin cytoskeleton
  • Glioma C6
  • Store-mediated Ca influx
  • Thapsigargin
  • UTP

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