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- W2014951331 abstract "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." @default.
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- W2014951331 date "2012-01-01" @default.
- W2014951331 modified "2023-09-25" @default.
- W2014951331 title "Mutant Soluble Ectodomain of Fibroblast Growth Factor Receptor-2 IIIc Attenuates Bleomycin-Induced Pulmonary Fibrosis in Mice" @default.
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- W2014951331 doi "https://doi.org/10.1248/bpb.35.731" @default.
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