徳島大学 教育・研究者情報データベース(EDB)

1. 木下 勝弘

   役割	任意
   貢献度	任意
   学籍番号	推奨

2. 青野 純典([徳島大学.大学院ヘルスバイオサイエンス研究部.医療創生科学部門.先端医療創生科学講座.呼吸器・膠原病内科学])

   役割	任意
   貢献度	任意
   学籍番号	推奨

3. 東 桃代([徳島大学.病院.中央診療施設等.感染制御部])

   役割	任意
   貢献度	任意
   学籍番号	推奨

4. 岸 潤

   役割	任意
   貢献度	任意
   学籍番号	推奨

5. (英) Takezaki Akio

   役割	任意
   貢献度	任意
   学籍番号	推奨

6. (英) Kishi Masami

   役割	任意
   貢献度	任意
   学籍番号	推奨

7. (英) Makino Hideki

   役割	任意
   貢献度	任意
   学籍番号	推奨

8. (英) Okazaki Hiroyasu

   役割	任意
   貢献度	任意
   学籍番号	推奨

9. 上原 久典([徳島大学.病院.中央診療施設等.病理部])

   役割	任意
   貢献度	任意
   学籍番号	推奨

10. 泉 啓介

    役割	任意
    貢献度	任意
    学籍番号	推奨

11. 曽根 三郎

    役割	任意
    貢献度	任意
    学籍番号	推奨

12. 西岡 安彦([徳島大学.大学院医歯薬学研究部.医学域.医科学部門.内科系.呼吸器・膠原病内科学])

    役割	任意
    貢献度	任意
    学籍番号	推奨

(英) Antifibrotic effects of focal adhesion kinase inhibitor in bleomycin-induced pulmonary fibrosis in mice.

(英) Focal adhesion kinase (FAK) is a nonreceptor tyrosine kinase involved in various biological functions, including cell survival, proliferation, migration, and adhesion. FAK is an essential factor for transforming growth factor to induce myofibroblast differentiation. In the present study, we investigated whether the targeted inhibition of FAK by using a specific inhibitor, TAE226, has the potential to regulate pulmonary fibrosis. TAE226 showed inhibitory activity of autophosphorylation of FAK at tyrosine 397 in lung fibroblasts. The addition of TAE226 inhibited the proliferation of lung fibroblasts in response to various growth factors, including platelet-derived growth factor and insulin-like growth factor I, in vitro. TAE226 strongly suppressed the production of type I collagen by lung fibroblasts. Furthermore, treatment of fibroblasts with TAE226 reduced the expression of -smooth muscle actin induced by transforming growth factor , indicating the inhibition of differentiation of fibroblasts to myofibroblasts. Administration of TAE226 ameliorated the pulmonary fibrosis induced by bleomycin in mice even when used late in the treatment. The number of proliferating mesenchymal cells was reduced in the lungs of TAE226-treated mice. These data suggest that FAK signal plays a significant role in the progression of pulmonary fibrosis and that it can become a promising target for therapeutic approaches to pulmonary fibrosis.

1. (英) Actins
2. (英) Animals
3. (英) Bleomycin
4. (英) Cell Differentiation
5. (英) Cell Proliferation
6. (英) Collagen Type I
7. (英) DNA
8. (英) Epithelial Cells
9. (英) Female
10. (英) Fibroblasts
11. (英) Focal Adhesion Kinase 1
12. (英) Insulin-Like Growth Factor I
13. (英) Mesenchymal Stromal Cells
14. (英) Mice
15. (英) Mice, Inbred C57BL
16. (英) Morpholines
17. (英) Myofibroblasts
18. (英) Phosphorylation
19. (英) Platelet-Derived Growth Factor
20. (英) Protein Kinase Inhibitors
21. (英) Pulmonary Fibrosis
22. (英) Transforming Growth Factor beta
23. (英) Tyrosine

1. (英) PublicationType: Journal Article

2. (英) PublicationType: Research Support, Non-U.S. Gov't