NDLI: Galectin-1 induced activation of the apoptotic death-receptor pathway in human Jurkat T lymphocytes

Content Provider	Springer Nature Link
Author	Brandt, Bettina Büchse, Tom Abou Eladab, Ehab Fathi Tiedge, Markus Krause, Eberhard Jeschke, Udo Walzel, Hermann
Copyright Year	2008
Abstract	Galectin-1 (gal-1), a member of the family of β-galactoside binding proteins, participates in several biological processes such as immunomodulation, cell adhesion, regulation of cell growth and apoptosis. The aim of this study was to investigate whether gal-1 interferes with the Fas (Apo-1/CD95)-associated apoptosis cascade in the T-cell lines Jurkat and MOLT-4. Gal-1 and an Apo-1 monoclonal antibody (mAb) induced DNA-fragmentation in Jurkat T-cells whereas MOLT-4 cells were resistant. Gal-1 stimulated DNA-fragmentation could be efficiently inhibited by caspase-8 inhibitor II (Z-IETD-FMK) and a neutralizing Fas mAb. Fas could be identified as a target for gal-1 recognition as demonstrated by immunofluorescence staining, binding of the receptor glycoprotein to immobilized gal-1 and analyses by immunoblotting as well as by liquid chromatography-tandem mass spectrometry (LC-MS/MS). Gal-1 stimulates the activation and proteolytic processing of procaspase-8 and downstream procaspase-3 in Jurkat-T cells. Inhibition of gal-1 induced procaspase-8 activation by a neutralizing Fas mAb strongly suggests that gal-1 recognition of Fas is associated with caspase-8 activation. Our data provide the first experimental evidence for targeting of gal-1 to glycotopes on Fas and the subsequent activation of the apoptotic death-receptor pathway.
Starting Page	599
Ending Page	609
Page Count	11
File Format	PDF
ISSN	09486143
Journal	Histochemistry and Cell Biology
Volume Number	129
Issue Number	5
e-ISSN	1432119X
Language	English
Publisher	Springer-Verlag
Publisher Date	2008-02-21
Publisher Place	Berlin/Heidelberg
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Galectin-1 T cell apoptosis Death receptor pathway Medicine/Public Health Anatomy
Content Type	Text
Resource Type	Article
Subject	Cell Biology Histology Molecular Biology Medical Laboratory Technology

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