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Related Experiment Videos

Mitochondria efficiently buffer subplasmalemmal Ca2+ elevation during agonist stimulation.

Roland Malli1, Maud Frieden, Karin Osibow

  • 1Department of Medical Biochemistry & Medical Molecular Biology, University of Graz, Austria.

The Journal of Biological Chemistry
|January 17, 2003
PubMed
Summary

Mitochondria and endoplasmic reticulum create distinct local calcium (Ca2+) domains in endothelial cells. This spatial regulation allows simultaneous activation of ion channels with opposing Ca2+ sensitivities, crucial for cell function.

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Area of Science:

  • Cellular Physiology
  • Ion Channel Regulation
  • Mitochondrial Function

Background:

  • Endothelial cells utilize local calcium (Ca2+) release from the endoplasmic reticulum (ER) to activate BK(Ca) channels.
  • Hyperpolarization induced by BK(Ca) channel activation promotes capacitative Ca2+ entry (CCE), which is paradoxically inhibited by high Ca2+ concentrations.

Purpose of the Study:

  • To investigate the roles of mitochondria and ER in regulating subplasmalemmal Ca2+ concentration ([Ca2+]pm).
  • To understand how coordinated activation of plasma membrane ion channels with opposing Ca2+ sensitivities is achieved.

Main Methods:

  • Cells were transfected with organelle-specific fluorescent markers (DsRed for mitochondria, yellow cameleon for ER).
  • Patch-clamp electrophysiology was used to measure local [Ca2+]pm near ER and mitochondria under varying conditions.

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  • Histamine stimulation was employed to induce Ca2+ release and entry.

    • Main Results:

    • Superficial ER and mitochondria establish distinct local Ca2+ microdomains.
    • Mitochondria actively buffer or lower local Ca2+ near the plasma membrane, while ER contributes to localized Ca2+ release.
    • Under physiological conditions, these domains enable simultaneous activation of BK(Ca) channels and CCE.

    Conclusions:

    • Superficial mitochondria and ER cooperate to generate spatially segregated domains of low and high Ca2+ concentration.
    • This compartmentalization is essential for the coordinated and differential activation of ion channels with opposing Ca2+ sensitivities, such as BK(Ca) channels and CCE pathways.