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* Division of Rheumatology, Children’s Hospital of Pittsburgh, University of Pittsburgh, School of Medicine, Pittsburgh, PA 15213;
Cincinnati Children’s Hospital Medical Center, Cincinnati, OH 45229;
Department of Cell Biology and Physiology, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261;
Department of Epidemiology, Graduate School of Public Health, Pittsburgh, PA 15261; and
¶ Department of Molecular Genetics and Biochemistry, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261
While analyzing gene expression in collagen-induced arthritis, we discovered that a poorly characterized gene, follistatin-like protein 1 (FSTL-1), is highly overexpressed in mouse paws during early arthritis, especially at the interface of synovial pannus and eroding bone. In this study, we show that FSTL-1 is a novel proinflammatory molecule with a previously unrecognized role in inflammation. Transfection of FSTL-1 into macrophages and fibroblasts leads to up-regulation of proinflammatory cytokines, including IL-1
, TNF-
, and IL-6. Overexpression of FSTL-1 in mouse paws by gene transfer results in severe paw swelling and arthritis.
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1 This work was supported in part by National Institutes of Health Grants AI44566 (to R.H) and AI 56374 (to P.D.R).
2 Address correspondence and reprint requests to Dr. Raphael Hirsch, Division of Rheumatology, Children’s Hospital of Pittsburgh, 3705 Fifth Avenue, Pittsburgh, PA 15213. E-mail address: raphael.hirsch{at}chp.edu
3 Abbreviations used in this paper: FSTL-1, follistatin-like protein 1; RA, rheumatoid arthritis; CII, type II collagen; CIA, collagen-induced arthritis.
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