Regular expression of discoidin domain receptor 2 in the improved adjuvant-induced animal model for rheumatoid arthritis.
- Author:
Wei LI
1
;
Yuan-qiang ZHANG
;
Xin-ping LIU
;
Li-bo YAO
;
Lan SUN
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Antibodies; blood; Arthritis, Experimental; etiology; metabolism; Arthritis, Rheumatoid; chemically induced; metabolism; BCG Vaccine; Collagen Type II; immunology; Discoidin Domain Receptors; Female; Fibroblasts; drug effects; metabolism; pathology; Freund's Adjuvant; Rats; Rats, Sprague-Dawley; Receptor Protein-Tyrosine Kinases; metabolism; Receptors, Mitogen; metabolism; Synovial Fluid; cytology; metabolism
- From: Chinese Medical Sciences Journal 2005;20(2):133-137
- CountryChina
- Language:English
-
Abstract:
OBJECTIVETo investigate the expression of discoidin domain receptor 2 (DDR2) of fibroblast-like synovial cells in improved adjuvant-induced animal (AIA) model for rheumatoid arthritis (RA) and to provide evidence for DDR2's antagonist use clinically.
METHODSAIA was modified by administrating 0.1 mL of complete Freund's adjuvant (CFA, mixed with 5 mg Bacillus Calmette-Guerin vaccine/mL) into rats' right hind paws and 0.125 mL tumor necrosis factor-alpha (2 U/mL) into right ankles and subpatellar fatty tissue. The expression of DDR2 in fibroblast-like synovial cells was assessed using immunohistochemistry, immunofluorescence histochemistry, and in situ hybridization methods. Levels of anti-collagen II antibody were measured using enzyme-linked immunosorbent assay.
RESULTSGiven the terms mentioned above, we found a more practical rat model, apparently decreasing immunization time (average 3-5 days). DDR2 can be detected upon the 15th day of immunization; expression gradually increased with time going on, and reaching a peak 35 days after immunization before gradually decreasing. Serum anti-collagen II antibody showed similar expression patterns as DDR2, but reached peak later than DDR2, about 40 days after immunization.
CONCLUSIONRegular expression of DDR2 in animal models infers its important role in the pathological process of RA.