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CD95 (Fas/Apo-1)-induced apoptosis results in loss of glucose transporter function

M V Berridge1, A S Tan, K D McCoy

  • 1Malaghan Institute of Medical Research, Wellington School of Medicine, Wellington, New Zealand.

Insights

CD95 ligation rapidly impairs glucose transport in T cells, preceding cell death. This early effect on glucose transporters occurs without nuclear signaling or new protein synthesis, suggesting a novel mechanism in apoptosis.

Area of Science:

  • Immunology
  • Cell Biology
  • Biochemistry

Background:

  • CD95 (Fas/Apo-1) ligand binding triggers apoptosis in activated human T cells.
  • Early molecular events leading to CD95-induced T cell death are not fully understood.

Purpose of the Study:

  • Investigate the impact of CD95 ligation on glucose transport and transporter function in activated T cells.
  • Elucidate the role of glucose transport regulation in early stages of CD95-mediated apoptosis.

Main Methods:

  • Utilized Jurkat cells as a model for activated human T cells.
  • Assessed glucose transport and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) responses following CD95 activation.
  • Analyzed glucose transporter (Glut 1) affinity and cell surface expression.

Main Results:

  • CD95 ligation rapidly reduced glucose transport capacity within minutes.
  • Short exposure to anti-CD95 antibodies (3 min) led to decreased glucose transport and MTT responses at 16 hours.
  • CD95 ligation decreased glucose transporter affinity for glucose without altering maximum velocity or Glut 1 surface expression.

Conclusions:

  • Acute regulation of glucose transport is an early effector mechanism in CD95-induced T cell death.
  • Early stages of CD95-mediated apoptosis may not require nuclear signaling or macromolecular synthesis.
  • CD95 ligation affects glucose transporter function, impacting cellular metabolism during apoptosis induction.

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