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Nitric oxide donor NOC-5 increases XIAP and Aven level in Jurkat cells

Elena G Starikova1, L A Tashireva, V V Novitsky

  • 1Siberian State Medical University of the Ministry of Health Care of the Russian Federation, 634055, Tomsk, Russia.

Cell Biology International
|March 29, 2014
PubMed

Insights

Nitric oxide (NO) treatment of Jurkat cells increased X-linked inhibitor of apoptosis protein (XIAP) and Aven levels. This increase may prevent caspase-9 activation following mitochondrial permeabilisation.

Area of Science:

  • Cellular biology
  • Molecular mechanisms of apoptosis

Background:

  • Nitric oxide (NO) plays a complex role in apoptosis.
  • Caspase-9 activation is a key event in the intrinsic apoptosis pathway.
  • Mitochondrial permeabilisation can trigger apoptosis.

Purpose of the Study:

  • To investigate the effect of NO on caspase-9 activity in Jurkat cells.
  • To examine the expression of apoptosis inhibitors XIAP and Aven in response to NO.

Main Methods:

  • Jurkat cells were treated with NO donors.
  • Mitochondrial permeabilisation was assessed.
  • Western blotting was used to quantify XIAP and Aven protein levels.

Main Results:

  • Mitochondrial permeabilisation occurred in NO-treated cells but did not activate caspase-9.
  • Levels of X-linked inhibitor of apoptosis protein (XIAP) and Aven were elevated in NO-treated cells.

Conclusions:

  • Increased XIAP and Aven expression may inhibit caspase-9 activation.
  • This mechanism could explain the lack of apoptosis despite mitochondrial permeabilisation in NO-treated Jurkat cells.
Keywords:
AvenXIAPapoptosiscaspasemitochondrianitric oxide

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