OBJECTIVE: To examine both the source of follistatin-like protein 1 (FSTL-1) and the factors that induce its expression in arthritis, and to determine whether juvenile rheumatoid arthritis (JRA) is characterized by overexpression of FSTL-1. METHODS: FSTL-1 expression patterns were analyzed by immunohistochemical staining of joint tissue derived from mice with collagen-induced arthritis. Induction of FSTL-1 secretion was assessed in osteoblasts, adipocytes, and human fibroblast-like synoviocytes in response to transforming growth factor beta (TGFbeta), interleukin-1beta (IL-1beta), tumor necrosis factor alpha (TNFalpha), and IL-6. In addition, sera and synovial fluid from children with oligoarticular, polyarticular, or systemic-onset JRA were assayed for FSTL-1 using a custom enzyme-linked immunosorbent assay. FSTL-1 concentrations in these patients were assessed for correlations with the erythrocyte sedimentation rate (ESR) and platelet count. RESULTS: Immunohistochemical staining of murine joint sections demonstrated expression of FSTL-1 in all cell types of the mesenchymal lineage, including osteocytes, chondrocytes, adipocytes, and fibroblasts. FSTL-1 could be induced in osteoblasts, adipocytes, and human fibroblast-like synoviocytes by TGFbeta, IL-1beta, TNFalpha, and IL-6. The IL-1beta response was significantly greater than the TNFalpha response (P < 0.05). In human serum and synovial fluid, only those samples from children with the systemic-onset JRA subtype had elevated concentrations of FSTL-1. The synovial fluid concentrations of FSTL-1 were 2-3-fold higher than the serum concentrations. The elevation in serum FSTL-1 concentrations seen in children with systemic-onset JRA correlated closely with elevations in the ESR and platelet count. CONCLUSION: These findings demonstrate that the arthritic joint matrix is a major source of FSTL-1 and that IL-1beta is a central mediator of FSTL-1 secretion. Furthermore, FSTL-1 may represent a useful biomarker of disease activity in systemic-onset JRA.
OBJECTIVE: To examine both the source of follistatin-like protein 1 (FSTL-1) and the factors that induce its expression in arthritis, and to determine whether juvenile rheumatoid arthritis (JRA) is characterized by overexpression of FSTL-1. METHODS:FSTL-1 expression patterns were analyzed by immunohistochemical staining of joint tissue derived from mice with collagen-induced arthritis. Induction of FSTL-1 secretion was assessed in osteoblasts, adipocytes, and human fibroblast-like synoviocytes in response to transforming growth factor beta (TGFbeta), interleukin-1beta (IL-1beta), tumor necrosis factor alpha (TNFalpha), and IL-6. In addition, sera and synovial fluid from children with oligoarticular, polyarticular, or systemic-onset JRA were assayed for FSTL-1 using a custom enzyme-linked immunosorbent assay. FSTL-1 concentrations in these patients were assessed for correlations with the erythrocyte sedimentation rate (ESR) and platelet count. RESULTS: Immunohistochemical staining of murine joint sections demonstrated expression of FSTL-1 in all cell types of the mesenchymal lineage, including osteocytes, chondrocytes, adipocytes, and fibroblasts. FSTL-1 could be induced in osteoblasts, adipocytes, and human fibroblast-like synoviocytes by TGFbeta, IL-1beta, TNFalpha, and IL-6. The IL-1beta response was significantly greater than the TNFalpha response (P < 0.05). In human serum and synovial fluid, only those samples from children with the systemic-onset JRA subtype had elevated concentrations of FSTL-1. The synovial fluid concentrations of FSTL-1 were 2-3-fold higher than the serum concentrations. The elevation in serum FSTL-1 concentrations seen in children with systemic-onset JRA correlated closely with elevations in the ESR and platelet count. CONCLUSION: These findings demonstrate that the arthritic joint matrix is a major source of FSTL-1 and that IL-1beta is a central mediator of FSTL-1 secretion. Furthermore, FSTL-1 may represent a useful biomarker of disease activity in systemic-onset JRA.
Authors: J T Cassidy; J E Levinson; J C Bass; J Baum; E J Brewer; C W Fink; V Hanson; J C Jacobs; A T Masi; J G Schaller Journal: Arthritis Rheum Date: 1986-02
Authors: D J Lovell; E H Giannini; A Reiff; G D Cawkwell; E D Silverman; J J Nocton; L D Stein; A Gedalia; N T Ilowite; C A Wallace; J Whitmore; B K Finck Journal: N Engl J Med Date: 2000-03-16 Impact factor: 91.245
Authors: Daniel J Lovell; Edward H Giannini; Andreas Reiff; Olcay Y Jones; Rayfel Schneider; Judyann C Olson; Leonard D Stein; Abraham Gedalia; Norman T Ilowite; Carol A Wallace; Mary Lange; Barbara K Finck; Daniel J Burge Journal: Arthritis Rheum Date: 2003-01
Authors: Brian T Campfield; Christi L Nolder; Anthony Marinov; Daniel Bushnell; Amy Davis; Caressa Spychala; Raphael Hirsch; Andrew J Nowalk Journal: Microb Pathog Date: 2014-04-24 Impact factor: 3.738
Authors: Masayuki Shimano; Noriyuki Ouchi; Kazuto Nakamura; Bram van Wijk; Koji Ohashi; Yasuhide Asaumi; Akiko Higuchi; David R Pimentel; Flora Sam; Toyoaki Murohara; Maurice J B van den Hoff; Kenneth Walsh Journal: Proc Natl Acad Sci U S A Date: 2011-10-10 Impact factor: 11.205
Authors: Matthew Henkel; Justin A Dutta; Jessica Partyka; Taylor Eddens; Raphael Hirsch; Jay K Kolls; Brian T Campfield Journal: Infect Immun Date: 2020-12-15 Impact factor: 3.441
Authors: Xuefeng B Ling; Jane L Park; Tanya Carroll; Khoa D Nguyen; Kenneth Lau; Claudia Macaubas; Edward Chen; Tzielan Lee; Christy Sandborg; Diana Milojevic; John T Kanegaye; Susanna Gao; Jane Burns; James Schilling; Elizabeth D Mellins Journal: Proteomics Date: 2010-11-23 Impact factor: 3.984
Authors: Mark Gorelik; Ndate Fall; Mekibib Altaye; Michael G Barnes; Susan D Thompson; Alexei A Grom; Raphael Hirsch Journal: J Rheumatol Date: 2013-05-15 Impact factor: 4.666
Authors: Yury Chaly; Yu Fu; Anthony Marinov; Bruce Hostager; Wei Yan; Brian Campfield; John A Kellum; Daniel Bushnell; Yudong Wang; Jerry Vockley; Raphael Hirsch Journal: Eur J Immunol Date: 2014-02-20 Impact factor: 5.532