Disease-specific Proteins from Rheumatoid Arthritis Patients.
10.3346/jkms.2006.21.3.478
- Author:
Choong Won KIM
1
;
Eun Hye CHO
;
Yun Jong LEE
;
Yoon Hee KIM
;
Young Sool HAH
;
Deok Ryong KIM
Author Information
1. Department of Biochemistry and RINS, College of Medicine and Institute of Health Sciences, Gyeongsang National University, Jinju, Korea. drkim@gsnu.ac.kr
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords:
Arthritis, Rheumatoid;
Autoantigens;
Fibronectins;
Proteomics
- MeSH:
Synovial Fluid/metabolism;
Sepharose/chemistry;
Proteomics/methods;
Middle Aged;
Male;
*Inflammation;
Humans;
*Gene Expression Regulation;
Female;
Collagen Type II/biosynthesis;
Autoantigens/metabolism;
Arthritis, Rheumatoid/*metabolism;
Aged;
Adult
- From:Journal of Korean Medical Science
2006;21(3):478-484
- CountryRepublic of Korea
- Language:English
-
Abstract:
Rheumatoid arthritis (RA) is a chronic inflammatiory disease that mainly destroys cartilages or bones at the joints. This inflammatory disorder is initiated by self-attack using own immune system, but the detail of pathological mechanism is unclear. Features of autoantigens leading to autoimmune disease are also under veil although several candidates including type II collagen have been suggested to play a role in pathogenesis. In this report, we tried to identify proteins responding to antibodies purified from RA patients and screen proteins up-regulated or down-regulated in RA using proteomic approach. Fibronectin, semaphorin 7A precursor, growth factor binding protein 7 (GRB7), and immunoglobulin mu chain were specifically associated with antibodies isolated from RA synovial fluids. In addition, some metabolic proteins such as adipocyte fatty acid binding protein, galectin-1 and apolipoprotein A1 precursor were overexpressed in RA synovium. Also, expression of peroxiredoxin 2 was up-regulated in RA. On the contrary, expression of vimentin was severely suppressed in RA synoviocytes. Such findings might give some insights into understanding of pathological mechanism in RA.
