Differential expression of WNTs and FRPs in the synovium of rheumatoid arthritis and osteoarthritis

被引:64
作者
Imai, Kazushi [1 ]
Morikawa, Masako
D'Armiento, Jeanine
Matsumoto, Hideo
Komiya, Koichiro
Okada, Yasunori
机构
[1] Nippon Dent Univ Tokyo, Sch Life Dent Tokyo, Dept Biochem, Tokyo, Japan
[2] Columbia Univ, Dept Med, New York, NY 10027 USA
[3] Keio Univ, Sch Med, Dept Orthoped Surg, Tokyo, Japan
[4] Keio Univ, Sch Med, Dept Pathol, Tokyo, Japan
关键词
arthritis; beta-catenin; FRP; osteoarthritis; rheumatoid arthritis; synovium; WNT;
D O I
10.1016/j.bbrc.2006.05.075
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 [生物化学与分子生物学]; 081704 [应用化学];
摘要
Synovial cells of the joint play a key role in the progression of rheumatoid arthritis (RA). However, the mechanism(s) that triggers aggression of RA synovial cells but not other arthropathies such as osteoarthritis (OA) is not clear. Here we examined expression of WNT and the WNT inhibitor, secreted frizzled-related protein (FRP), in RA and OA synovium by reverse transcription-PCR. WNT10B was most frequently detected in RA synovium, and FRP1, FRP2, and FRP4 in OA synovium. Immunohistochemistry localized WNT10B and FRP1 in synovial lining cells, fibroblasts, and endothelial cells in RA and OA synovium, respectively, and WNT10B expression was increased in parallel with the degree of inflammatory cell infiltration and tissue fibrosis. Membrane-type 1 matrix metalloprotemse (MT1MMP) was upregulated by WNT10B and activation of WNT signaling. MT1MMP immunolocalized to cells identical to WNT10B and P-catenin staining. The present study demonstrated that WNTs and FRPs are differentially expressed in RA and OA synovium, and suggests an involvement in the pathology of these diseases. (c) 2006 Elsevier Inc. All rights reserved.
引用
收藏
页码:1615 / 1620
页数:6
相关论文
共 32 条
[1]
Mechanisms of disease: Cytokine pathways and joint inflammation in rheumatoid arthritis. [J].
Choy, EHS ;
Panayi, GS .
NEW ENGLAND JOURNAL OF MEDICINE, 2001, 344 (12) :907-916
[2]
LOCALIZATION OF TUMOR-NECROSIS-FACTOR-ALPHA IN SYNOVIAL TISSUES AND AT THE CARTILAGE PANNUS JUNCTION IN PATIENTS WITH RHEUMATOID-ARTHRITIS [J].
CHU, CQ ;
FIELD, M ;
FELDMANN, M ;
MAINI, RN .
ARTHRITIS AND RHEUMATISM, 1991, 34 (09) :1125-1132
[3]
Evolving concepts of rheumatoid arthritis [J].
Firestein, GS .
NATURE, 2003, 423 (6937) :356-361
[4]
SYNOVIAL-MEMBRANE HISTOPATHOLOGY IN DIFFERENTIAL-DIAGNOSIS OF RHEUMATOID-ARTHRITIS, GOUT, PSEUDOGOUT, SYSTEMIC LUPUS-ERYTHEMATOSUS, INFECTIOUS ARTHRITIS AND DEGENERATIVE JOINT DISEASE [J].
GOLDENBERG, DL ;
COHEN, AS .
MEDICINE, 1978, 57 (03) :239-252
[5]
The Frizzled family: receptors for multiple signal transduction pathways [J].
Huang, HC ;
Klein, PS .
GENOME BIOLOGY, 2004, 5 (07)
[6]
Ijiri K, 2002, J RHEUMATOL, V29, P2266
[7]
Secreted Frizzled-related proteins: searching for relationships and patterns [J].
Jones, SE ;
Jomary, C .
BIOESSAYS, 2002, 24 (09) :811-820
[8]
Kimura Y, 1999, INT J CANCER, V84, P174, DOI 10.1002/(SICI)1097-0215(19990420)84:2<174::AID-IJC14>3.0.CO
[9]
2-E
[10]
The development of clinical signs of rheumatoid synovial inflammation is associated with increased synthesis of the chemokine CXCL8 (interleukin-8) [J].
Kraan, MC ;
Patel, DD ;
Haringman, JJ ;
Smith, MD ;
Weedon, H ;
Ahern, MJ ;
Breedveld, FC ;
Tak, PP .
ARTHRITIS RESEARCH, 2001, 3 (01) :65-71