Skip Navigation


Glycobiology Advance Access first published online on February 23, 2005
This version published online on March 8, 2005
Glycobiology, doi:10.1093/glycob/cwi050
This Article
Right arrow Advance Access manuscript (PDF) Freely available
Right arrow All Versions of this Article:
15/7/7C    most recent
cwi050v2
cwi050v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Tjew, S. L.
Right arrow Articles by Johnson, P.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Tjew, S. L.
Right arrow Articles by Johnson, P.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The Author 2005. Published by Oxford University Press. All rights reserved. For permissions, please e-mail: journals.permissions@oupjournals.org
Received December 16, 2004
Revised February 10, 2005
Accepted February 15, 2005

Article

Expression of N-acetylglucosamine 6-O sulfotransferases (GlcNAc6STs) -1 and -4 in human monocytes: GlcNAc6ST-1 is implicated in the generation of the 6-sulfo N-acetyllactosamine/Lewis x epitope on CD44 and is induced by TNF-{alpha}

Sie Lung Tjew 1, Kelly L. Brown 1, Reiji Kannagi 2, and Pauline Johnson 1*

1 Department of Microbiology and Immunology, University of British Columbia, #300-6174, University Boulevard, Vancouver, B.C., V6T 1Z3, Canada and
2 Program of Experimental Pathology, Aichi Cancer Center, Nagoya 464, Japan

* To whom correspondence should be addressed.
Pauline Johnson, E-mail: pauline{at}interchange.ubc.ca


  Abstract

Sulfation at the 6-O position of N-acetylglucosamine (GlcNAc) in the context of sialyl 6-sulfo Lewis x occurs constitutively on specific glycoproteins present on high-walled endothelial venules (HEV) and is important for L-selectin dependent homing of lymphocytes. Here, the pro-inflammatory cytokine, TNF-{alpha}, induced the expression of 6-sulfo N-acetyllactosamine (LacNAc)/Lewis x on human peripheral blood monocytes (PBM). This epitope was detected by mAb AG107 after neuraminidase treatment suggesting a sialylated epitope, which was present on the cell adhesion molecule, CD44. Treatment of human PBM with TNF-{alpha} upregulated the expression of GlcNAc6ST-1 and GlcNAc6ST-4, as determined by RT-PCR. However, only GlcNAc6ST-1 was induced by TNF-{alpha} in the human SR91 cell line, which also upregulated the AG107 epitope. In ECV304 cells, expression of GlcNAc6ST-4 alone was insufficient to generate the AG107 epitope. However, transfection of GlcNAc6ST-1 resulted in significant sulfate incorporation into CD44 and generated the 6-sulfo LacNAc/Lewis x epitope on CD44, which was present largely on Nlinked glycans. This demonstrates the induction of GlcNAc6STs in human monocytes in response to TNF-{alpha} and implicates GlcNAc6ST-1 in the generation of the 6-sulfo LacNAc/Lewis x epitope on CD44.

Keywords: carbohydrate sulfation/CD44/inflammation/monocytes/sulfotransferase.
All the betas in this article have been changed to alphas.
Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 J. Biol. Chem.Home page
N. Kimura, K. Ohmori, K. Miyazaki, M. Izawa, Y. Matsuzaki, Y. Yasuda, H. Takematsu, Y. Kozutsumi, A. Moriyama, and R. Kannagi
Human B-lymphocytes Express {alpha}2-6-Sialylated 6-Sulfo-N-acetyllactosamine Serving as a Preferred Ligand for CD22/Siglec-2
J. Biol. Chem., November 2, 2007; 282(44): 32200 - 32207.
[Abstract] [Full Text] [PDF]


Disclaimer:
Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.