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Annexin V counteracts apoptosis while inducing Ca(2+) influx in human lymphocytic T cells

C Gidon-Jeangirard1, E Solito, A Hofmann

  • 1Institut d'Hématologie et d'Immunologie, Faculté de Médecine, Université Louis Pasteur, Strasbourg, 67085, France.

Insights

Annexin V delays apoptosis by increasing intracellular calcium (Ca2+) in T cells. This mechanism involves regulating membrane permeability and requires the N-terminal domain of annexin V for its protective effect.

Area of Science:

  • Cell Biology
  • Immunology
  • Biochemistry

Background:

  • Annexin V has been previously shown to delay apoptosis.
  • Apoptosis involves DNA cleavage, release of membrane particles, and caspase-3 processing.

Purpose of the Study:

  • To investigate the mechanism by which annexin V counteracts apoptosis in human CEM T cells.
  • To determine the role of intracellular calcium (Ca2+) in annexin V-mediated apoptosis inhibition.

Main Methods:

  • Measuring intracellular Ca2+ concentration ([Ca2+]i) in CEM T cells treated with annexin V.
  • Utilizing EGTA to reduce extracellular Ca2+ concentration.
  • Employing modified annexins with altered electrophysiological properties.

Main Results:

  • Annexin V's anti-apoptotic effect correlated with increased [Ca2+]i.
  • Reduced extracellular Ca2+ abolished annexin V's protective effect.
  • The N-terminal domain of annexin V was essential for its Ca2+-dependent anti-apoptotic action.

Conclusions:

  • Annexin V promotes Ca2+ influx, leading to increased [Ca2+]i.
  • Calcium acts as an inhibitor of apoptosis in CEM T cells.
  • Annexin V protects against apoptosis by modulating membrane Ca2+ permeability and elevating [Ca2+]i.

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