PT  - JOURNAL ARTICLE
AU  - Chrong-Reen Wang
AU  - Shih-Yao Chen
AU  - Ai-Li Shiau
AU  - Chao-Liang Wu
AU  - I-Ming Jou
AU  - Lee Chao
AU  - Julie Chao
TI  - Upregulation of kallistatin expression in rheumatoid joints.
DP  - 2007 Nov 01
TA  - The Journal of Rheumatology
PG  - 2171--2176
VI  - 34
IP  - 11
4099  - http://www.jrheum.org/content/34/11/2171.short
4100  - http://www.jrheum.org/content/34/11/2171.full
SO  - J Rheumatol2007 Nov 01; 34
AB  - OBJECTIVE: Previous studies demonstrated suppression of rat ankle arthritis by local injection of kallistatin gene, a negative regulator of angiogenesis. We analyzed circulating levels, synovial concentrations, and tissue localizations of kallistatin in patients with rheumatoid arthritis (RA). METHODS: Paired plasma and joint fluid samples were simultaneously obtained from 24 patients with RA and 14 with osteoarthritis (OA). Synovial tissues from 5 patients with RA and 5 with OA were obtained during surgery. Fibroblast-like synoviocytes (FLS) and mononuclear cells (MNC) were prepared. ELISA was used to measure kallistatin levels of plasma, joint fluid, cell lysate, and synovium homogenate extract. Synovial tissues were subjected to Western blot and immunohistochemical staining. In addition, the tissue kallikrein (TK) levels of plasma and joint fluid samples were also measured by the ELISA. RESULTS: Circulating and synovial levels of kallistatin and TK were elevated in patients with RA. The immunohistochemical assay exhibited stainings of kallistatin on both infiltrating MNC and FLS. Intracellular kallistatin levels were significantly elevated in MNC and FLS from patients with RA. CONCLUSION: Elevated kallistatin levels were demonstrated in patients with RA, particularly in synovial tissues, FLS, and MNC. This report is the first to demonstrate upregulation of kallistatin expression in rheumatoid joints.