Mutant Soluble Ectodomain of Fibroblast Growth Factor Receptor-2 IIIc Attenuates Bleomycin-Induced Pulmonary Fibrosis in Mice

DOI Web Site Web Site PubMed 被引用文献1件 参考文献19件
  • Yu Zhi-hong
    Institute of Bioengineering, College of Life Science and Technology, Jinan University
  • Wang Ding-ding
    Department of Biotechnology, Institute of Life Science and Biological Pharmacy, Guangdong Pharmaceutical University
  • Zhou Zhi-you
    Institute of Bioengineering, College of Life Science and Technology, Jinan University
  • He Shui-lian
    Institute of Bioengineering, College of Life Science and Technology, Jinan University
  • Chen An-an
    Institute of Bioengineering, College of Life Science and Technology, Jinan University
  • Wang Ju
    Institute of Bioengineering, College of Life Science and Technology, Jinan University

この論文をさがす

抄録

We have developed a strong inhibitor (S252W mutant soluble ectodomain of fibroblast growth factor recptor-2 IIIc, msFGFR2) that binds FGFs strongly and blocks the activation of FGFRs. In vitro, msFGFR2 could inhibit the promoting effect of transforming growth factor (TGF)-β1 on the proliferation of primary lung fibroblasts. In vivo, msFGFR2 alleviated lung fibrosis through inhibiting the expression of α-smooth muscle actin (SMA) and collagen deposit. In Western blotting of the right lung tissues and immunohistochemical assay, we found the level of p-FGFRs, p-mitogen activated protein kinase (MAPK) and p-Smad3 in the mice of bleomycin (BLM) group treated with msFGFR2 was down dramatically compared with the mice of BLM group, which suggested the activations of FGF and TGF-β signals were blocked meanwhile. In summary, msFGFR2 attenuated BLM-induced fibrosis and is an attractive therapeutic candidate for human pulmonary fibrosis.

収録刊行物

被引用文献 (1)*注記

もっと見る

参考文献 (19)*注記

もっと見る

キーワード

詳細情報 詳細情報について

問題の指摘

ページトップへ