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Rheumatology 1999; 38: 1195-1202
© 1999 British Society for Rheumatology

Autocrine induction of gliostatin/platelet-derived endothelial cell growth factor (GLS/PD-ECGF) and GLS-induced expression of matrix metalloproteinases in rheumatoid arthritis synoviocytes

H. Muro, Y. Waguri-Nagaya, Y. Mukofujiwara, T. Iwahashi, T. Otsuka, N. Matsui, A. Moriyama2, K. Asai1 and T. Kato1

Department of Orthopaedic Surgery and
1 Department of Bioregulation Research, Nagoya City University Medical School and
2 Division of Biomolecular Science, Institute of Natural Sciences, Nagoya City University, Mizuho-ku, Nagoya 467–8601, Japan

Correspondence to: Y. Waguri-Nagaya, Department of Orthopaedic Surgery, Nagoya City University, Medical School, Mizuho-Ku, Nagoya 467–8601, Japan.

Objective. The purpose of this study was to examine how gliostatin/platelet-derived endothelial cell growth factor (GLS/PD-ECGF) is involved in the molecular mechanism of cartilage degradation in rheumatoid arthritis (RA) with special reference to the GLS-induced gene expression and protein synthesis of matrix metalloproteinase (MMP)-1 (collagenase-1) and MMP-3 (stromelysin-1).

Methods. Fibroblast-like synoviocytes (FLSs) obtained from RA patients were cultured and stimulated by GLS. Changes in the expression levels of GLS, MMP-1 and MMP-3 were assessed by Northern blot analysis and reverse transcription-polymerase chain reaction (RT-PCR) for GLS, and by RT-PCR and enzyme-linked immunosorbent assay for MMPs and tissue inhibitor of metalloproteinase 1.

Results. GLS demonstrated a self-induction of mRNA in cultured RA FLSs. GLS evoked a dose-dependent induction of MMP-1 and MMP-3 mRNAs, and subsequently their extracellular secretion.

Conclusion. These findings suggest that GLS is a plausible pathogenic factor causing the extensive joint destruction in RA mediated via MMPs.

KEY WORDS: Gliostatin, Platelet-derived endothelial cell growth factor, Thymidine phosphorylase, Rheumatoid arthritis, Matrix metalloproteinase.


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