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Role of fibroblast growth factor-10 and -7 in idiopathic interstitial pneumonia

Research Project

Project/Area Number 16590766
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Respiratory organ internal medicine
Research InstitutionNippon Medical School

Principal Investigator

FUKUDA Yuh  Nippon Medical School, Graduate School of Medicine, Professor, 大学院・医学研究科, 教授 (60097037)

Co-Investigator(Kenkyū-buntansha) ISHIZAKI Masamichi  Nippon Medical School, Department of Medicine, Associate Professor, 医学部, 助教授 (40096954)
NAKAYAMA Tomoko  Nippon Medical School, Department of Medicine, Research Associate, 医学部, 助手 (50350038)
Project Period (FY) 2004 – 2005
Project Status Completed (Fiscal Year 2005)
Budget Amount *help
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2005: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 2004: ¥2,600,000 (Direct Cost: ¥2,600,000)
Keywordsusual interstitial pneumonia / nonspecific interstitial pneumonia / fibroblast growth factor 10 / fibroblast growth factor 7 / fibroblast growth factor receptor / early fibrotic focus / microdissection / real time PCR / realtime PCR / 特発性器質化肺炎
Research Abstract

Idiopathic interstitial pneumonia is interstitial pneumonia due to unknown cause and includes usual interstitial pneumonia (UIP), nonspecific interstitial pneumonia (NSIP), cryptogenic organizing pneumonia (COP) et al. and similar disease to interstitial pneumonia is diffuse alveolar damage (DAD). Fibroblast growth factor (FGF)-10 is mainly produced by mesenchymal cells and is known as an important growth and development factor for epithelial cells. We investigated FGF10, FGF7 and their receptor FGFR in UIP, NSIP, COP and DAD. Immunohistochemical distribution and stainability of FGF10 and FGFR were studied. The amount of FGF10, FGF7 and FGFR in whole specimens and microdissected early fobrotic lesions were measured with real time PCR. Immunohistochemistry showed FGF10 was positive in mesenchymal cells of early fibrotic lesions of UIP, NSIP, COP and DAD. Regenerated epithelial cells covering on early fibrotic lesions in UIP were squamous metaplastic cells and those of NSIP, COP and DAD were type II alveolar epithelial cells, and all of them were positive for FGFR. Real time PCR showed FGF10 was relatively higher in the specimens of interstitial pneumonia compared to control, but FGF7 was similar level in them. The ratio of FGF10 to FGFR with microdissected early fibrotic lesions was lower in UIP compared to COP. These results showed that FGF 10 and FGFR were involved in the mechanisms of repair in the early fibrotic lesions of interstitial pneumonia, and FGF10/FGFR may correlate with the impaired alveolar epithelial cell regeneration in UIP.

Report

(3 results)
  • 2005 Annual Research Report   Final Research Report Summary
  • 2004 Annual Research Report
  • Research Products

    (2 results)

All 2006 2005

All Journal Article (2 results)

  • [Journal Article] びまん性肺胞傷害における線維化と筋線維芽細胞.2006

    • Author(s)
      居来提托乎提, 中山智子, 石崎正通, 福田 悠
    • Journal Title

      日本医科大学雑誌 2,1

      Pages: 18-24

    • NAID

      130004941850

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2005 Annual Research Report 2005 Final Research Report Summary
  • [Journal Article] Fibrosis and myofibroblast in diffuse alveolar damage.2005

    • Author(s)
      Tohote, J., Nakayama, T., Ishizaki, M., Fukuda, Y.
    • Journal Title

      NIHON IKA DAIGAKU IGAKUKAI ZASSHI 2

      Pages: 18-24

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2005 Final Research Report Summary

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Published: 2004-04-01   Modified: 2016-04-21  

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