Journal of Biochemistry Advance Access published online on December 13, 2006
Journal of Biochemistry, doi:10.1093/jb/mvm019
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
© 2006 The Japanese Biochemical Society
Characterization of Galectin-9-Induced Death of Jurkat T-Cells
1Department of Endocrinology, Faculty of Medicine, Kagawa University, Kagawa, Japan
2Department of Cell Regulation, Faculty of Medicine, Kagawa University, Kagawa, Japan
3Department of Immunology and Immunopathology, Faculty of Medicine, Kagawa University, Kagawa, Japan
4Galpharma Co., Inc., Kagawa, Japan
Prof. Takanori Nakamura, Ph. D. Department of Endocrinology, Faculty of Medicine, Kagawa University, 1750-1 Ikenobe, Miki-cho, Kita-gun, Kagawa 761-0793, Japan. TEL: + 81-87-891-2106 FAX: + 81-87-891-2108 E-mail: tnaka{at}med.kagawa-u.ac.jp
Received October 18, 2006; Accepted November 22, 2006
 |
Abstract |
|---|
Galectin-9, a mammalian lectin with affinity for ß–galactosides, is known as an apoptosis inducer of activated T lymphocytes. In the present study, we examined the properties of galectin–9–mediated cell death of Jurkat T–cells. Galectin–9NC (wild–type), consisting of two CRDs (N–terminal and C–terminal carbohydrate recognition domains), and derivatives of it, galectins–9–NN and –9–CC, induced Jurkat T–cell apoptosis. However, a single CRD (galectin–9NT or –CT) had no effect, suggesting the stable dimeric structure of two CRDs is required for the activity. The apoptosis was inhibited by pretreatment with an N–glycan synthesis inhibitor, indicating that the expression of N–glycans in the cells is essential for galectin–9–induced apoptosis. We previously showed that the apoptosis of MOLT–4 cell is mediated by galectin–9 via a Ca2+–calpain–caspase–1–dependent pathway. In Jurkat cells, the cell death by galectin–9, was insufficiently suppressed by caspase inhibitors, Ca2+–chelator or calpain inhibitor. Furthermore, we observed the loss of mitochondrial membrane potential and significant AIF release in galectin–9–treated cells. These findings suggest that caspase–dependent and –independent death pathways exist in Jurkat cells, and the main pathway might vary with the T–cell type.
Key Words: galectin–9, galectin, apoptosis, Jurkat, T–cell
CiteULike 
Connotea 
Del.icio.us What's this?
This article has been cited by other articles:
|
|
 |
|
  W. Peng, H. Y. Wang, Y. Miyahara, G. Peng, and R.-F. Wang Tumor-Associated Galectin-3 Modulates the Function of Tumor-Reactive T Cells Cancer Res., September 1, 2008; 68(17): 7228 - 7236. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Bi, L. A. Earl, L. Jacobs, and L. G. Baum Structural Features of Galectin-9 and Galectin-1 That Determine Distinct T Cell Death Pathways J. Biol. Chem., May 2, 2008; 283(18): 12248 - 12258. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. Yamamoto, N. Nishi, H. Shoji, A. Itoh, L.-H. Lu, M. Hirashima, and T. Nakamura Induction of Cell Adhesion by Galectin-8 and its Target Molecules in Jurkat T-Cells J. Biochem., March 1, 2008; 143(3): 311 - 324. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 E. Nutku-Bilir, S. A. Hudson, and B. S. Bochner Interleukin-5 Priming of Human Eosinophils Alters Siglec-8 Mediated Apoptosis Pathways Am. J. Respir. Cell Mol. Biol., January 1, 2008; 38(1): 121 - 124. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. V. Tribulatti, J. Mucci, V. Cattaneo, F. Aguero, T. Gilmartin, S. R. Head, and O. Campetella Galectin-8 Induces Apoptosis in the CD4highCD8high Thymocyte Subpopulation Glycobiology, December 1, 2007; 17(12): 1404 - 1412. [Abstract] [Full Text] [PDF]
|
|