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Activation of caspases and mitochondria in FTY720-mediated apoptosis in human T cell line Jurkat

M Fujino1, X K Li, L Guo

  • 1Department of Experimental Surgery and Bioengineering, National Children's Medical Research Center, Tokyo, Japan.

International Immunopharmacology
|October 19, 2001
PubMed

Insights

FTY720 induces apoptosis in human T cells by activating caspases and disrupting mitochondria. This immunosuppressive drug

Area of Science:

  • Immunology
  • Cell Biology
  • Pharmacology

Background:

  • FTY720 is an immunosuppressive drug known to induce lymphocyte apoptosis.
  • Its precise mechanism, particularly the roles of caspases and mitochondria, requires further elucidation.

Purpose of the Study:

  • To investigate the involvement of caspases and mitochondria in FTY720-induced apoptosis.
  • To determine the sequence of events in FTY720-mediated cell death using Jurkat cells.

Main Methods:

  • Treatment of Jurkat cells with FTY720.
  • Assay of caspase activation (caspases 1-10).
  • Measurement of mitochondrial membrane potential, cytochrome c release, and phosphatidylserine exposure.
  • Use of a caspase inhibitor (Z-Asp-CH2-DCB) to probe the apoptotic pathway.

Main Results:

  • FTY720 activated caspases 2, 3, 6, 8, 9, and 10, but not caspases 1 or 5.
  • FTY720 treatment led to loss of mitochondrial membrane potential, cytochrome c release, and phosphatidylserine externalization.
  • The caspase inhibitor blocked apoptosis and phosphatidylserine externalization but not mitochondrial events.

Conclusions:

  • FTY720 induces apoptosis through a pathway involving caspase activation and mitochondrial dysfunction.
  • Mitochondrial events appear to precede or initiate caspase activation in FTY720-treated cells.
  • Caspases likely act downstream of mitochondrial pathway activation in FTY720-mediated apoptosis.

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