Sialic acids linked to glycoconjugates of Fas regulate the caspase-9-dependent and mitochondria-mediated pathway of Fas-induced apoptosis in Jurkat T cell lymphoma

  • Authors:
    • Osamu Suzuki
    • Yoshihiro Nozawa
    • Masafumi Abe
  • View Affiliations

  • Published online on: September 1, 2003     https://doi.org/10.3892/ijo.23.3.769
  • Pages: 769-774
Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

To clarify the functions of sialic acids linked to glycoconjugates of Fas in Fas-induced apoptosis, Jurkat T cells, untreated and treated with neuraminidase, were incubated with anti-Fas monoclonal antibody, CH11. Apoptosis of Jurkat T cells induced by incubation with CH11 was enhanced by the pre-treatment with neuraminidase. By flow cytometry sialylated glycoconjugates were detected on the cell surface of Jurkat T cells using LFA lectin, which specifically reacts with sialic acid, and pre-treatment with Vibrio Cholerae neuraminidase resulted in desialylation of Jurkat cell surface glycoconjugates. The enhancement of Fas-induced apoptosis by pre-treatment with neuraminidase was inhibited by z-VAD-fmk, a broad caspase inhibitor, and Ac-LEHD-CHO, an inhibitor of caspase-9, but not by Ac-IETD-CHO an inhibitor of caspase-8 or 6, imipramine, an inhibitor of acidic sphingomyelinase, glutathione, an inhibitor of neutral sphingomyelinase and Fumonisin B1, an inhibitor of ceramide synthase. Mitochondrial membrane potentials (Δψm) measured with a Mitocapture assay kit demonstrated that the loss of Δψm involved in Fas-induced apoptosis was enhanced by pre-treatment with neuraminidase. Furthermore, Western blot analysis using polyclonal antibody (C-20) against Fas detected Fas at about 45 kDa, and pre-treatment with neuraminidase resulted in a reduction of the molecular weight of Fas of about 8 kDa. These data suggest that the enhancement of Fas-induced apoptosis by pre-treatment with neuraminidase was mediated by a caspase-9 dependent pathway closely associated with the loss of Δψm, not by activation of caspase-8, -6 or acidic and neutral sphingomyelinases, and that sialic acid linked to glycoconjugates of Fas may regulate Fas-induced apoptosis in human T cell lymphoma.

Related Articles

Journal Cover

September 2003
Volume 23 Issue 3

Print ISSN: 1019-6439
Online ISSN:1791-2423

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
x
Spandidos Publications style
Suzuki O, Nozawa Y and Abe M: Sialic acids linked to glycoconjugates of Fas regulate the caspase-9-dependent and mitochondria-mediated pathway of Fas-induced apoptosis in Jurkat T cell lymphoma. Int J Oncol 23: 769-774, 2003
APA
Suzuki, O., Nozawa, Y., & Abe, M. (2003). Sialic acids linked to glycoconjugates of Fas regulate the caspase-9-dependent and mitochondria-mediated pathway of Fas-induced apoptosis in Jurkat T cell lymphoma. International Journal of Oncology, 23, 769-774. https://doi.org/10.3892/ijo.23.3.769
MLA
Suzuki, O., Nozawa, Y., Abe, M."Sialic acids linked to glycoconjugates of Fas regulate the caspase-9-dependent and mitochondria-mediated pathway of Fas-induced apoptosis in Jurkat T cell lymphoma". International Journal of Oncology 23.3 (2003): 769-774.
Chicago
Suzuki, O., Nozawa, Y., Abe, M."Sialic acids linked to glycoconjugates of Fas regulate the caspase-9-dependent and mitochondria-mediated pathway of Fas-induced apoptosis in Jurkat T cell lymphoma". International Journal of Oncology 23, no. 3 (2003): 769-774. https://doi.org/10.3892/ijo.23.3.769