徳島大学 教育・研究者情報データベース(EDB)

1. (英) Kishi Masami

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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])

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3. 佐藤 正大([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]/[徳島大学.病院.診療科.内科.呼吸器・膠原病内科])

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4. (英) Koyama Kazuya

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5. 東 桃代

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6. (英) Abe Shuichi

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7. 河野 弘([徳島大学.大学院医歯薬学研究部.医学域.連携研究部門(医学域).寄附講座系(医学域).地域リウマチ・総合内科学])

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8. 岸 潤

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9. 豊田 優子

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10. (英) Okazaki Hiroyasu

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11. 小川 博久([徳島大学.大学院医歯薬学研究部.医学域.医科学部門.病理系.疾患病理学])

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12. 上原 久典([徳島大学.病院.診療科.病理診断科])

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13. 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])

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(英) Blockade of platelet-derived growth factor receptor-β, not receptor-α ameliorates bleomycin-induced pulmonary fibrosis in mice.

(英) Platelet-derived growth factor (PDGF) has been implicated in the pathogenesis of pulmonary fibrosis. Nintedanib, a multi-kinase inhibitor that targets several tyrosine kinases, including PDGF receptor (PDGFR), was recently approved as an anti-fibrotic agent to reduce the deterioration of FVC in patients with idiopathic pulmonary fibrosis (IPF). However, the effects of PDGFR-α or -β on pulmonary fibrosis remain unclear. In an attempt to clarify their effects, we herein used blocking antibodies specific for PDGFR-α (APA5) and -β (APB5) in a bleomycin (BLM)-induced pulmonary fibrosis mouse model. The effects of these treatments on the growth of lung fibroblasts were examined using the 3H-thymidine incorporation assay in vitro. The anti-fibrotic effects of these antibodies were investigated with the Ashcroft score and collagen content of lungs treated with BLM. Their effects on inflammatory cells in the lungs were also analyzed using bronchoalveolar lavage fluid. We investigated damage to epithelial cells and the proliferation of fibroblasts in the lungs. APA5 and APB5 inhibited the phosphorylation of PDGFR-α and -β as well as the proliferation of lung fibroblasts induced by PDGF-AA and BB. The administration of APB5, but not APA5 effectively inhibited BLM-induced pulmonary fibrosis in mice. Apoptosis and the proliferation of epithelial cells and fibroblasts were significantly decreased by the treatment with APB5, but not by APA5. The late treatment with APB5 also ameliorated fibrosis in lungs treated with BLM. These results suggest that PDGFR-α and -β exert different effects on BLM-induced pulmonary fibrosis in mice. A specific approach using the blocking antibody for PDGFR-β may be useful for the treatment of pulmonary fibrosis.

1. (英) PublicationType: Journal Article