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Caspase-dependent inhibition of store-operated Ca(2+) entry into apoptosis-committed Jurkat cells

Marta Onopiuk1, Katarzyna Wierzbicka, Wojciech Brutkowski

  • 1Department of Biochemistry, The Nencki Institute of Experimental Biology, Warsaw, Poland.

Biochemical and Biophysical Research Communications
|July 21, 2010
PubMed

Insights

Fas receptor activation in T-cells reduces STIM1 and Orai1 proteins during apoptosis. This inhibits calcium entry, potentially protecting cells from necrosis.

Area of Science:

  • Immunology
  • Cell Biology
  • Calcium Signaling

Background:

  • T-cell activation initiates calcium signaling crucial for immune responses.
  • Fas ligand expression limits immune response by inducing apoptosis in activated T-cells.
  • Store-operated calcium (SOC) entry is inhibited in apoptotic cells.

Purpose of the Study:

  • To investigate the mechanism of SOC entry inhibition in T-cells undergoing Fas receptor-mediated apoptosis.
  • To determine the role of STIM1 and Orai1 proteins in this process.

Main Methods:

  • Activation of Fas receptor in Jurkat T-cells.
  • Assessment of STIM1 and Orai1 protein levels.
  • Measurement of calcium (Ca2+) entry.
  • Caspase activity assays.

Main Results:

  • Fas receptor activation led to a caspase-dependent decrease in STIM1 and Orai1 protein levels in T-cells.
  • This reduction in STIM1 and Orai1 correlated with significant inhibition of Ca2+ entry.
  • The observed inhibition of Ca2+ entry occurred in Jurkat cells undergoing apoptosis.

Conclusions:

  • Fas receptor activation induces apoptosis in T-cells by reducing STIM1 and Orai1, thereby inhibiting store-operated calcium entry.
  • This mechanism may serve as a protective measure against calcium overload and subsequent necrosis during apoptosis.

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