Skip Navigation



Rheumatology Advance Access published online on June 27, 2003

Rheumatology, doi:10.1093/rheumatology/keg385
Rheumatology © British Society for Rheumatology 2003; all rights reserved
This Article
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
42/11/1383    most recent
keg385v1
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 Foell, D.
Right arrow Articles by Roth, J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Foell, D.
Right arrow Articles by Roth, J.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© 2003 Rheumatology 42 © British Society for Rheumatology 2003; all rights reserved

Original Papers

Expression of the pro-inflammatory protein S100A12 (EN-RAGE) in rheumatoid and psoriatic arthritis

D. Foell 1*, D. Kane 2, B. Bresnihan 2, T. Vogl 3, W. Nacken 3, C. Sorg 3, O. FitzGerald 2, and J. Roth 1

1 Department of Paediatrics; Institute of Experimental Dermatology, University of Münster, Germany
2 Department of Rheumatology, St. Vincent's University Hospital, Dublin, Republic of Ireland
3 Institute of Experimental Dermatology, University of Münster, Germany

* Corresponding author. E-mail: dfoell{at}uni.

Received 13 November 2002 ; accepted 5 March 2003

Abstract

Objectives. Infiltration of synovial tissue by neutrophils is crucial in rheumatoid arthritis (RA), psoriatic arthritis (PsA) and seronegative arthritis (SA). Altered vascular function and endothelial activation are important in PsA. S100A12 (EN-RAGE) is secreted by activated granulocytes and binds to the receptor for advanced glycation end products, which induces nuclear factor (NF)-{kappa}B-dependent activation of endothelium.

Methods. Immunohistochemical studies were performed to detect synovial S100A12 expression. We analysed serum and synovial fluid of 42 patients for S100A12 levels.

Results. S100A12 was strongly expressed in inflamed synovial tissue whereas it was nearly undetectable in synovia of controls or patients after successful treatment. Serum levels of S100A12 correlated with disease activity.

Conclusions. Local expression of S100A12 in inflamed tissue suggests a role in synovitis, especially in PsA. High serum concentrations of S100A12 in patients with active arthritis compared with healthy controls or patients in remission point to its usefulness as a serum marker.

Key words: S100A12, RAGE, Calgranulin C, Neutrophils, Synovitis, Psoriatic arthritis.
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
Rheumatology (Oxford)Home page
L. Oslejskova, M. Grigorian, H. Hulejova, J. Vencovsky, K. Pavelka, J. Klingelhofer, S. Gay, M. Neidhart, H. Brabcova, D. Suchy, et al.
Metastasis-inducing S100A4 protein is associated with the disease activity of rheumatoid arthritis
Rheumatology, October 14, 2009; (2009) kep316v1.
[Abstract] [Full Text] [PDF]


Home page
Rheumatology (Oxford)Home page
C. A. Davies, A. L. Herrick, L. Cordingley, A. J. Freemont, and M. Jeziorska
Expression of advanced glycation end products and their receptor in skin from patients with systemic sclerosis with and without calcinosis
Rheumatology, August 1, 2009; 48(8): 876 - 882.
[Abstract] [Full Text] [PDF]


Home page
Rheumatology (Oxford)Home page
R. Pullerits, H. F. d'Elia, A. Tarkowski, and H. Carlsten
The decrease of soluble RAGE levels in rheumatoid arthritis patients following hormone replacement therapy is associated with increased bone mineral density and diminished bone/cartilage turnover: a randomized controlled trial
Rheumatology, July 1, 2009; 48(7): 785 - 790.
[Abstract] [Full Text] [PDF]


Home page
J. Immunol.Home page
B. Moser, D. D. Desai, M. P. Downie, Y. Chen, S. F. Yan, K. Herold, A. M. Schmidt, and R. Clynes
Receptor for Advanced Glycation End Products Expression on T Cells Contributes to Antigen-Specific Cellular Expansion In Vivo
J. Immunol., December 15, 2007; 179(12): 8051 - 8058.
[Abstract] [Full Text] [PDF]


Home page
Rheumatology (Oxford)Home page
R. Pullerits, M. Bokarewa, L. Dahlberg, and A. Tarkowski
Synovial fluid expression of autoantibodies specific for RAGE relates to less erosive course of rheumatoid arthritis
Rheumatology, August 1, 2007; 46(8): 1367 - 1371.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Respir. Crit. Care Med.Home page
I. Campo, P. Morbini, M. Zorzetto, C. Tinelli, E. Brunetta, C. Villa, C. Bombieri, M. Cuccia, C. Agostini, V. Bozzi, et al.
Expression of Receptor for Advanced Glycation End Products in Sarcoid Granulomas
Am. J. Respir. Crit. Care Med., March 1, 2007; 175(5): 498 - 506.
[Abstract] [Full Text] [PDF]


Home page
Rheumatology (Oxford)Home page
M. M. C. Steenvoorden, A. H. M. van der Helm-van Mil, G. Stoeken, R. A. Bank, R. R. P. DeVries, T. W. J. Huizinga, J. DeGroot, and R. E. M. Toes
The RAGE G82S polymorphism is not associated with rheumatoid arthritis independently of HLA-DRB1*0401
Rheumatology, April 1, 2006; 45(4): 488 - 490.
[Full Text] [PDF]


Home page
J. Cell Sci.Home page
P. Most, M. Boerries, C. Eicher, C. Schweda, M. Volkers, T. Wedel, S. Sollner, H. A. Katus, A. Remppis, U. Aebi, et al.
Distinct subcellular location of the Ca2+-binding protein S100A1 differentially modulates Ca2+-cycling in ventricular rat cardiomyocytes
J. Cell Sci., January 15, 2005; 118(2): 421 - 431.
[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.