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TRIC channels supporting efficient Ca(2+) release from intracellular stores.

Elisa Venturi1, Rebecca Sitsapesan, Daiju Yamazaki

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|December 18, 2012
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Trimeric intracellular cation-selective (TRIC) channels, TRIC-A and TRIC-B, are crucial for calcium release from intracellular stores. Their dysfunction in knockout mice leads to hypertension, respiratory failure, and heart defects, highlighting their essential physiological roles.

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Area of Science:

  • Cellular Biology
  • Ion Channel Physiology
  • Molecular Medicine

Background:

  • Trimeric intracellular cation-selective (TRIC) channels, TRIC-A and TRIC-B, are located in the sarco/endoplasmic reticulum and nuclear membranes.
  • TRIC-A is highly expressed in excitable tissues, while TRIC-B is found in various tissues at lower levels.
  • These channels form homo-trimeric assemblies and conduct monovalent cations.

Purpose of the Study:

  • To investigate the physiological roles of TRIC-A and TRIC-B channels.
  • To elucidate the contribution of TRIC channels to calcium release from intracellular stores.
  • To understand the pathophysiological consequences of TRIC channel defects.

Main Methods:

  • Electrophysiological recordings in lipid bilayer reconstitution systems.
  • Analysis of TRIC-A and TRIC-B knockout mouse models.
  • Assessment of calcium handling in various cell types and tissues from knockout mice.

Main Results:

  • TRIC channels exhibit cation selectivity and function similarly to potassium channels under intracellular conditions.
  • Tric-a-knockout mice display hypertension due to impaired vascular smooth muscle cell calcium release.
  • Tric-b-knockout mice exhibit respiratory failure from defective surfactant handling in alveolar cells.
  • Double knockout mice show embryonic heart failure with disrupted cardiomyocyte calcium handling.

Conclusions:

  • TRIC channels are essential for regulating calcium release from intracellular stores, partly by mediating counter-potassium movements.
  • TRIC-A and TRIC-B play distinct but critical roles in maintaining cardiovascular, respiratory, and cardiac functions.
  • Dysfunction of TRIC channels leads to severe pathophysiological conditions, underscoring their therapeutic potential.