2-Aminoethoxydiphenyl borate inhibits agonist-induced Ca2+ signals by blocking inositol trisphosphate formation in acutely dissociated mouse pancreatic acinar cells

Jie Wu, Teruko Takeo, Sechiko Suga, Takahiro Kanno, Tomohiro Osanai, Katsuhiko Mikoshiba, Makoto Wakui

Research output: Contribution to journalArticlepeer-review

19 Scopus citations

Abstract

Evidence suggests that 2-aminoethoxydiphenyl borate (2-APB) modulates intracellular Ca2+ signals in a complex manner. 2-APB inhibits or potentiates intracellular Ca2+ signals in different cell types, perhaps through different mechanisms. Here, we report a novel mechanism underlying 2-APB-induced inhibition of agonist-activated Ca2+ oscillations in mouse pancreatic acinar cells, using patch-clamp and biochemical techniques. Pre-treatment of the cells with 100 μM 2-APB completely abolished ACh-but not inositol trisphosphate (InsP3)-induced Ca 2+ oscillations, suggesting that the mechanism of inhibition occurs between cytoplasmic receptors and InsP3 receptor activation. In addition, 100 μM 2-APB significantly inhibited ACh-induced phospholipase C (PLC) activation. These findings indicate that, in mouse pancreatic acinar cells, in addition to modulating InsP3 receptors and blocking the store-operated Ca2+ pathway, high concentrations of 2-APB also inhibit agonist-induced Ca2+ signals by reducing InsP3 formation.

Original languageEnglish (US)
Pages (from-to)592-595
Number of pages4
JournalPflugers Archiv European Journal of Physiology
Volume448
Issue number6
DOIs
StatePublished - Sep 2004
Externally publishedYes

Keywords

  • 2-Aminoethoxydiphenyl borate (2-APB)
  • Calcium oscillation
  • Calcium stores
  • Inositol 1,4,5-trisphosphate
  • Mouse
  • Pancreatic acinar cells
  • Patch-clamp
  • Phospholipase C (PLC)

ASJC Scopus subject areas

  • Physiology
  • Clinical Biochemistry
  • Physiology (medical)

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