Advertisement
J. Lipid Res.
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
QUICK SEARCH:   [advanced]


     

A more recent version of this article appeared on November 1, 2008

Papers In Press, published online ahead of print July 24, 2008
J. Lipid Res., doi:10.1194/jlr.M800143-JLR200
This Article
Right arrow Full Text (Accepted Manuscript)
Right arrow All Versions of this Article:
M800143-JLR200v1
49/11/2323    most recent
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
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 Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Google Scholar
Right arrow Articles by Zhao, C.
Right arrow Articles by Bourgoin, S. G.
PubMed
Right arrow PubMed Citation
Right arrow Articles by Zhao, C.
Right arrow Articles by Bourgoin, S. G.
Social Bookmarking
Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati  
What's this?

Submitted on March 17, 2008
Revised on July 18, 2008
Accepted on July 23, 2008

Specific and overlapping sphingosine-1-phosphate receptor functions in human synoviocytes: impact of TNF-alpha

Chenqi Zhao, Maria J. Fernandes, Mélanie Turgeon, Sabrina Tancrède, John Di Battista, Patrice E. Poubelle, and Sylvain G. Bourgoin

Anatomie et Physiologie, Université Laval, Québec, Québec G1V 4G2

Corresponding Author: sylvain.bourgoin{at}crchul.ulaval.ca

Sphingosine-1-phosphate (S1P), via interaction with its G protein-coupled receptors, regulates various physiological and pathological responses. The present study investigated the role of S1P/S1P receptor signaling in several functional responses of human fibroblast-like synoviocytes (FLS) that may contribute to the pathogenesis of rheumatoid arthritis (RA). We report that FLS express the S1P1, S1P2 and S1P3 receptors. Moreover, exogenously applied S1P induces FLS 1) migration, 2) secretion of inflammatory cytokine/chemokine, and 3) protection from apoptosis. Using specific S1P receptor agonists/antagonists, we determined that S1P stimulates FLS migration through S1P1 and S1P3, induces cytokine/chemokine secretion through S1P2 and S1P3, whereas protects from cell apoptosis via S1P1. The S1P-mediated cell motility and cytokine/chemokine secretion seem to be regulated by the p38 mitogen-activated protein kinase (MAPK), p42/44 MAPK and Rho kinase signal transduction pathways. Interestingly, treatment of FLS with TNF-a increases S1P3 expression and correlates with the enhancement of S1P-induced cytokine/chemokine production. Our data suggest that S1P1, S1P2, and S1P3 play essential roles in the pathogenesis of RA by modulating FLS migration, cytokine/chemokine production, and cell survival. Moreover, the cytokine-rich environment of the inflamed synovium may synergize with S1P signaling to exacerbate the clinical manifestations of this autoimmune disease.


Add to CiteULike CiteULike   Add to Complore Complore   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati    What's this?


This article has been cited by other articles:


Home page
 J. Lipid Res.Home page
W. B. Bollag
Potential role of sphingosine 1-phosphate in the pathogenesis of rheumatoid arthritis
J. Lipid Res., November 1, 2008; 49(11): 2281 - 2282.
[Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
 All ASBMB Journals   Journal of Biological Chemistry 
 Molecular and Cellular Proteomics   ASBMB Today 
Copyright © 2008 by the American Society for Biochemistry and Molecular Biology.
Advertisement
spacer
Advertisement
Advertisement