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Imatinib ameliorates bronchiolitis obliterans via inhibition of fibrocyte migration and differentiation
http://hdl.handle.net/2297/46841
http://hdl.handle.net/2297/46841b9a4cc12-cee0-4d65-951a-7f87462c0d18
名前 / ファイル | ライセンス | アクション |
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ME-PR-WATANABE-S-138.pdf (626.0 kB)
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Item type | 学術雑誌論文 / Journal Article(1) | |||||
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公開日 | 2017-12-05 | |||||
タイトル | ||||||
タイトル | Imatinib ameliorates bronchiolitis obliterans via inhibition of fibrocyte migration and differentiation | |||||
言語 | ||||||
言語 | eng | |||||
資源タイプ | ||||||
資源タイプ識別子 | http://purl.org/coar/resource_type/c_6501 | |||||
資源タイプ | journal article | |||||
著者 |
Watanabe, Satoshi
× Watanabe, Satoshi× Kasahara, Kazuo× Waseda, Yuko× Takato, Hazuki× Nishikawa, Shingo× Yoneda, Taro× Hara, Johsuke× Sone, Takashi× Abo, Miki× Kimura, Hideharu× Nakao, Shinji |
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書誌情報 |
Journal of Heart and Lung Transplantation 巻 36, 号 2, p. 138-147, 発行日 2017-02-01 |
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ISSN | ||||||
収録物識別子タイプ | ISSN | |||||
収録物識別子 | 1053-2498 | |||||
NCID | ||||||
収録物識別子タイプ | NCID | |||||
収録物識別子 | AA10796579 | |||||
DOI | ||||||
関連タイプ | isVersionOf | |||||
識別子タイプ | DOI | |||||
関連識別子 | 10.1016/j.healun.2016.06.001 | |||||
出版者 | ||||||
出版者 | Elsevier | |||||
抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | Background: Imatinib, a tyrosine kinase inhibitor, has been proposed as a potential anti-fibrotic agent for fibroproliferative diseases, including bronchiolitis obliterans (BO). However, the underlying anti-fibrotic mechanisms of the agent remain unclear. We evaluated whether bone (BM)-derived progenitor cells, fibrocytes, might be a target of imatinib in the attenuation of BO. Methods: We used a murine BO model induced by heterotopic tracheal transplantation and assessed the origin of fibroblasts by using green fluorescent protein-BM chimeric mice. We also evaluated the effects of imatinib on luminal obstruction and fibrocyte accumulation. The effects of imatinib on fibrocyte migration and differentiation were assessed by culturing fibrocytes in vitro. Results: In the murine BO model, tracheal allografts showed epithelial injury and developed complete luminal occlusion 28 days after transplantation. Most of the mesenchymal cells that had accumulated in the tracheal allograft were derived from BM cells. Imatinib treatment ameliorated the airway luminal occlusion and significantly reduced the number of fibrocytes in the allografts. In vitro studies showed that imatinib inhibited migration of cultured blood fibrocytes via the platelet-derived growth factor/platelet-derived growth factor receptor axis. Imatinib also inhibited differentiation of fibrocytes via suppression of c-Abl activity that was essential for the differentiation of monocytes to fibrocytes. Conclusions: Imatinib prevents airway luminal obstruction by inhibiting the migration and differentiation of fibrocytes. Fibrocytes may be a novel target in the prevention and treatment of BO. © 2016 International Society for Heart and Lung Transplantation. | |||||
内容記述 | ||||||
内容記述タイプ | Other | |||||
内容記述 | Embargo Period 12 months | |||||
権利 | ||||||
権利情報 | Copyright © Elsevier (CC-BY NC ND) | |||||
著者版フラグ | ||||||
出版タイプ | AM | |||||
出版タイプResource | http://purl.org/coar/version/c_ab4af688f83e57aa |