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2000 Fiscal Year Final Research Report Summary

Gliostatin as a clinical marker of rheumatoid arthritis and its regulation

Research Project

Project/Area Number 10470309
Research Category

Grant-in-Aid for Scientific Research (B).

Allocation TypeSingle-year Grants
Section一般
Research Field Orthopaedic surgery
Research InstitutionNagoya City University

Principal Investigator

MATSUI Nobuo  Nagoya City University, Medical School, Professor, 医学部, 教授 (40009569)

Co-Investigator(Kenkyū-buntansha) ASAI Kiyofumi  Nagoya City University, Medical School, Associate Professor, 医学部, 助教授 (70212462)
NAGAYA Yuko  Nagoya City University, Medical School, Research Associate, 医学部, 助手 (90291583)
OTSUKA Takanobu  Nagoya City University, Medical School, Assistant professor, 医学部, 講師 (10185316)
Project Period (FY) 1998 – 2000
Keywordsgliostatin / platelet-derived endothelial cell growth factor / thymidine phosphorylase / rheumatoid arthritis / synoviocytes / rabbit / matrix metalloproteinases
Research Abstract

Neovascularization, proliferation of synovial cells, and mononuclear cell influx and activation are characteristic events observed in synovial joints in the pathohistology of rheumatoid arthritis (RA). The purposes of this study are to examine how gliostatin/platelet derived-endothelial cell growth factor (GLS/PD-ECGF) is involved in the molecular mechanism of cartilage degradation in 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) and to examine synovial inflammation in rabbit knees induced by intraarticular administration of human GLS/PD-ECGF.
GLS demonstrated a self induction of mRNA in cultured RA synoviocytes. GLS evoked a dose-dependent induction of MMP-1 and MMP-3 mRNAs and subsequently their extracellular secretions. Intraarticular injection of rHuGLS resulted in development of diffuse synovitis resembling rheumatoid arthritis. The mutant protein which was prepared by site-directed mutagenesis and lacking dThdPase activity also brought out the same effect.
These findings suggest that GLS is a plausible pathogenic factor causing the extensive joint destruction in RA mediated via MMPs and that human GLS can cause RA-like synovitis in rabbit knee joints via a mechanism other than its thymidine phosphorylase activity.

  • Research Products

    (6 results)

All Other

All Publications (6 results)

  • [Publications] Mukofujwara Y, et al.: "Abnormal glycosilation of IgG as a clinical parametic in patients with RA : Its constitutional analysis by HPLC"J Cli Biochem Nutr.. 25. 131-142 (1998)

    • Description
      「研究成果報告書概要(和文)」より
  • [Publications] Muro H, et al.: "Autocrine induction of GLS/PD-ECGF and GLS-induced expression of MMPs in RA synoviocytes'"Rheumatol. 38. 1195-1202 (1999)

    • Description
      「研究成果報告書概要(和文)」より
  • [Publications] Woguri-Nagaya Y, et al.: "Synovial inflamonation and hyperplasia induced by GLS/Pb-ECGF in rabbit knees"Rheumatol Int. 20. 13-19 (2000)

    • Description
      「研究成果報告書概要(和文)」より
  • [Publications] Mukofujiwara Y, et al.: "Abnormal glycosilation of IgG as a clinical parameter in patients with rheumatoid arthritis : Its constitutional analysis by HPLC."J Clin Biochem Nutr. 25. 131-142 (1998)

    • Description
      「研究成果報告書概要(欧文)」より
  • [Publications] Muro H, et al.: "Autocrine induction of gliostatin/platelet-derived endothelial cell growth factor (GLS/PD-ECGF) and GLS-induced expression of matrix metalloproteinases in rheumatoid arthritis synoviocytes."Rheumatol. 38. 1195-1202 (1999)

    • Description
      「研究成果報告書概要(欧文)」より
  • [Publications] Waguri-Nagaya Y, et al.: "Synovial inflammation and hyperplasia induced by gliostatin/platelet-derived endothelial cell growth factor in rabbit knees."Rheumatol Int. 20. 13-19 (2000)

    • Description
      「研究成果報告書概要(欧文)」より

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Published: 2002-03-26  

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