Upregulation of kallistatin expression in rheumatoid joints

Chrong-Reen Wang, Shih Yao Chen, Ai-Li Shiau, Chao-Liang Wu, I. Ming Jou, Lee Chao, Julie Chao

Research output: Contribution to journalArticle

18 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)2171-2176
Number of pages6
JournalJournal of Rheumatology
Volume34
Issue number11
Publication statusPublished - 2007 Nov

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Up-Regulation
Joints
Rheumatoid Arthritis
Fibroblasts
Tissue Kallikreins
Osteoarthritis
Enzyme-Linked Immunosorbent Assay
Staining and Labeling
kallistatin
Synovial Membrane
Ankle
Arthritis
Western Blotting
Injections
Synoviocytes
Genes

All Science Journal Classification (ASJC) codes

  • Rheumatology
  • Immunology

Cite this

Wang, C-R., Chen, S. Y., Shiau, A-L., Wu, C-L., Jou, I. M., Chao, L., & Chao, J. (2007). Upregulation of kallistatin expression in rheumatoid joints. Journal of Rheumatology, 34(11), 2171-2176.
Wang, Chrong-Reen ; Chen, Shih Yao ; Shiau, Ai-Li ; Wu, Chao-Liang ; Jou, I. Ming ; Chao, Lee ; Chao, Julie. / Upregulation of kallistatin expression in rheumatoid joints. In: Journal of Rheumatology. 2007 ; Vol. 34, No. 11. pp. 2171-2176.
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abstract = "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.",
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Wang, C-R, Chen, SY, Shiau, A-L, Wu, C-L, Jou, IM, Chao, L & Chao, J 2007, 'Upregulation of kallistatin expression in rheumatoid joints', Journal of Rheumatology, vol. 34, no. 11, pp. 2171-2176.

Upregulation of kallistatin expression in rheumatoid joints. / Wang, Chrong-Reen; Chen, Shih Yao; Shiau, Ai-Li; Wu, Chao-Liang; Jou, I. Ming; Chao, Lee; Chao, Julie.

In: Journal of Rheumatology, Vol. 34, No. 11, 11.2007, p. 2171-2176.

Research output: Contribution to journalArticle

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AU - Wang, Chrong-Reen

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AU - Shiau, Ai-Li

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N2 - 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.

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.

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