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Apoptotic volume decrease, pH acidification and chloride channel activation during apoptosis requires CD45 expression

G Dupéré-Minier1, C Hamelin, P Desharnais

  • 1INRS-Institut Armand-Frappier, Pointe-Claire, Quebec H9R 1G6, Canada.

Apoptosis : an International Journal on Programmed Cell Death
|August 18, 2004
PubMed
Summary
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Loss of CD45 expression in leukemia cells inhibits nuclear apoptosis by disrupting chloride channel regulation and ionic homeostasis. This impacts DNA fragmentation and DFF40 activation.

Area of Science:

  • Cell Biology
  • Molecular Oncology
  • Immunology

Background:

  • Mitochondrial-perturbating agents induce apoptosis.
  • Loss of CD45 expression in HPB-ALL cells inhibits nuclear apoptosis.
  • CD45 is implicated in regulating Src family proto-oncogenes crucial for apoptosis.

Purpose of the Study:

  • To investigate the role of CD45 in nuclear apoptosis.
  • To explore the significance of chloride efflux in DNA fragmentation.
  • To determine the involvement of tyrosine kinase in chloride channel regulation.

Main Methods:

  • Comparison of CD45-deficient (CD45-) and normal (CD45+) lymphocytes.
  • Analysis of ionic homeostasis and chloride channel phosphorylation.
  • Assessment of DNA fragmentation under varying osmotic conditions (hypertonic and hypotonic media).

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Main Results:

  • CD45-deficient lymphocytes exhibit disturbed ionic homeostasis compared to normal lymphocytes.
  • Chloride channel phosphorylation is significantly inhibited in CD45-deficient cells, while expression levels remain similar.
  • Hypertonic medium inhibits DNA fragmentation in CD45+ cells; hypotonic medium increases it in CD45- cells.

Conclusions:

  • CD45 plays a critical role in nuclear apoptosis.
  • CD45 regulates chloride channels essential for cellular ionic homeostasis.
  • Proper ionic balance, mediated by CD45 and chloride channels, is vital for DFF40 activation and DNA fragmentation.