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Related Experiment Videos

2,5-Di-(tert-butyl)-1,4-benzohydroquinone and cyclopiazonic acid decrease the Ca2+ permeability of endoplasmic

L Missiaen1, H De Smedt, G Droogmans

  • 1Laboratorium voor Fysiologie, K.U. Leuven Campus Gasthuisberg, Belgium.

European Journal of Pharmacology
|December 1, 1992
PubMed
Summary

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The endoplasmic-reticulum Ca2+ pump inhibitor tBuBHQ reduces passive Ca2+ leak from internal stores. This finding indicates tBuBHQ and cyclopiazonic acid are not specific tools for studying receptor-mediated Ca2+ entry.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Physiology

Background:

  • Endoplasmic-reticulum Ca2+ pumps regulate intracellular calcium (Ca2+) levels.
  • Store depletion is a key mechanism for studying Ca2+ permeability across plasma membranes.
  • Specific inhibitors are crucial for dissecting Ca2+ signaling pathways.

Purpose of the Study:

  • To investigate the effect of Ca2+ pump inhibitors on passive Ca2+ leak from intracellular stores.
  • To determine if 2,5-di-(tert-butyl)-1,4-benzohydroquinone (tBuBHQ) and other inhibitors can be used as specific tools to study receptor-mediated Ca2+ entry.

Main Methods:

  • Utilized permeabilized A7r5 vascular smooth-muscle cells.
  • Assessed passive Ca2+ leak from internal stores using various Ca2+ pump inhibitors, including tBuBHQ, cyclopiazonic acid, and thapsigargin.

Related Experiment Videos

  • Measured inositol 1,4,5-trisphosphate-mediated Ca2+ release.

    • Main Results:

    • tBuBHQ significantly reduced passive Ca2+ leak from internal stores at concentrations typically used to empty stores in intact cells.
    • Cyclopiazonic acid showed a similar, though less pronounced, effect on reducing Ca2+ leak.
    • Thapsigargin did not affect passive Ca2+ leak, and inositol 1,4,5-trisphosphate-mediated Ca2+ release remained unaltered by these inhibitors.

    Conclusions:

    • tBuBHQ and cyclopiazonic acid exhibit non-specific effects on passive Ca2+ leak, limiting their utility as specific probes for receptor-mediated Ca2+ entry.
    • The findings necessitate a re-evaluation of the specificity of these commonly used Ca2+ pump inhibitors in Ca2+ signaling research.
    • Further studies are needed to identify specific pharmacological tools for investigating Ca2+ entry mechanisms.