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Annexin V counteracts apoptosis while inducing Ca2+ influx in human lymphocytic T cells

  1. Author:
    Gidon-Jeangirard, C.
    Solito, E.
    Hofmann, A.
    Russo-Marie, F.
    Freyssinet, J. M.
    Martinez, M. C.

  2. Author Address

    Martinez MC Univ Strasbourg 1, Fac Med, Inst Hematol & Immunol 4 Rue Kirschleger F-67085 Strasbourg France Univ Strasbourg 1, Fac Med, Inst Hematol & Immunol F-67085 Strasbourg France Hop Bicetre, INSERM, U143 F-94275 Le Kremlin Bicetre France Inst Cochin Genet Mol, INSERM, U332 F-75014 Paris France Frederick Canc Res & Dev Ctr Frederick, MD USA
    1. Year: 1999
  2. Journal: Biochemical and Biophysical Research Communications
    1. 265
    2. 3
    3. Pages: 709-715
  4. Type of Article: Article
  1. Abstract:

    We have previously shown that when annexin V is present during the execution of a cell death program, apoptosis is delayed. This is reflected by the inhibition of DNA cleavage and of the release of apoptotic membrane particles, and by reduction of the proteolytic processing of caspase-3. Here, we have studied the mechanism(s) through which annexin V counteracts apoptosis in the human CEM. T cell line. The degree of apoptosis inhibition was associated with an increase of intracellular Ca2+ concentration ([Ca2+](i)). Reduction of the extracellular Ca2+ concentration by EG;TA abolished the anti-apoptotic effect, suggesting that annexin V favors Ca2+ influx and that Ca2+ acts as an inhibitor rather than an activator of apoptosis in CEM: T cells. The effects on apoptosis and [Ca2+](i) of several modified annexins with different electrophysiological properties indicate that the N-terminal domain of annexin V is necessary for the Ca2+-dependent anti-apoptotic action of annexin V. These results suggest that annexin V regulates membrane Ca2+ permeability and is protective against apoptosis by increasing [Ca2+](i) in CEM T cells. (C) 1999 Academic Press. [References: 41]

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