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Related Experiment Videos

Store-operated Ca2+ entry depends on mitochondrial Ca2+ uptake.

Maike D Glitsch1, Daniel Bakowski, Anant B Parekh

  • 1Department of Physiology, University of Oxford, Parks Road, Oxford OX1 3PT, UK.

The EMBO Journal
|December 18, 2002
PubMed
Summary

Mitochondria regulate store-operated calcium channels by maintaining an energized state. Mitochondrial depolarization inhibits calcium influx, revealing a novel regulatory role in cellular calcium signaling.

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Area of Science:

  • Cellular Biology
  • Physiology
  • Mitochondrial Function

Background:

  • Store-operated calcium channels (SOCCs) are crucial for cellular calcium influx, activated by depleted intracellular calcium stores.
  • Mitochondria play a role in calcium homeostasis by buffering calcium released by inositol trisphosphate (InsP3).
  • Energized mitochondria are typically required for InsP3 to effectively trigger SOCC activation under physiological conditions.

Purpose of the Study:

  • To investigate the novel role of mitochondria in regulating SOCCs under physiological conditions.
  • To determine the mechanism by which mitochondrial function impacts SOCC activity.
  • To explore the potential crosstalk between mitochondria and SOCCs.

Main Methods:

  • Investigated the effect of mitochondrial depolarization on SOCC activity.

Related Experiment Videos

  • Assessed SOCC influx independently of store depletion methods.
  • Differentiated mitochondrial effects from calcium-dependent inactivation and other cellular signaling pathways (ATP, oxidants, pH, NO, mPTP).
  • Examined the impact of impaired mitochondrial calcium uptake on SOCC function.

    • Main Results:

    • Mitochondrial depolarization suppresses SOCC influx regardless of the mechanism of store depletion.
    • This suppression is independent of mitochondrial roles in InsP3-sensitive store depletion.
    • The observed effect is distinct from calcium-dependent inactivation of SOCCs.
    • The mechanism does not involve changes in ATP, oxidants, cytosolic acidification, nitric oxide, or the mitochondrial permeability transition pore.
    • Suppression of SOCC influx is alleviated when mitochondrial calcium uptake is impaired.

    Conclusions:

    • Mitochondria have a novel, direct role in regulating SOCCs under physiological conditions.
    • Mitochondrial depolarization inhibits SOCC influx through a mechanism independent of store depletion and known inactivation pathways.
    • Impaired mitochondrial calcium uptake prevents this inhibitory effect, suggesting a role for mitochondrial calcium handling.
    • These findings suggest a fundamental role for mitochondria in controlling calcium influx and raise the possibility of bidirectional calcium-dependent crosstalk between mitochondria and SOCCs.