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Suppression of fibrogenic gene expression and liver fibrosis using a synthetic prostacyclin agonist
https://doi.org/10.24517/00027387
https://doi.org/10.24517/000273878501c5a8-48c6-4b44-87e0-c6462e893319
| 名前 / ファイル | ライセンス | アクション |
|---|---|---|
CA-PR-MATSUMOTO-K-241.pdf (1.7 MB)
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| Item type | 学術雑誌論文 / Journal Article(1) | |||||||||||
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| 公開日 | 2017-10-05 | |||||||||||
| タイトル | ||||||||||||
| タイトル | Suppression of fibrogenic gene expression and liver fibrosis using a synthetic prostacyclin agonist | |||||||||||
| 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 | |||||||||||
| ID登録 | ||||||||||||
| ID登録 | 10.24517/00027387 | |||||||||||
| ID登録タイプ | JaLC | |||||||||||
| 著者 |
Xu, Qing
× Xu, Qing× Sakai, Katsuya× Nakayama, Mizuho× Suzuki, Yoshinori× Tambo, Chikako× 松本, 邦夫 |
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| 著者別表示 |
酒井, 克也
× 酒井, 克也
× 中山, 瑞穂
× 松本, 邦夫
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| 提供者所属 | ||||||||||||
| 内容記述タイプ | Other | |||||||||||
| 内容記述 | 金沢大学がん進展制御研究所 | |||||||||||
| 書誌情報 |
Biomedical Research (Japan) 巻 34, 号 5, p. 241-250, 発行日 2013-01-01 |
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| ISSN | ||||||||||||
| 収録物識別子タイプ | ISSN | |||||||||||
| 収録物識別子 | 0388-6107 | |||||||||||
| NCID | ||||||||||||
| 収録物識別子タイプ | NCID | |||||||||||
| 収録物識別子 | AA00110128 | |||||||||||
| DOI | ||||||||||||
| 関連タイプ | isIdenticalTo | |||||||||||
| 識別子タイプ | DOI | |||||||||||
| 関連識別子 | 10.2220/biomedres.34.241 | |||||||||||
| 出版者 | ||||||||||||
| 出版者 | Biomedical Research Press | |||||||||||
| 抄録 | ||||||||||||
| 内容記述タイプ | Abstract | |||||||||||
| 内容記述 | Chronic injury and inflammation in the liver are associated with the development of liver fibrosis. Expressions of transforming growth factor-β1 (TGF-β1) and hepatocyte growth factor (HGF) participate in the development and suppression, respectively, of liver fibrosis. Here, we investigated the effect of ONO-1301, a synthetic prostaglandin I2/IP receptor agonist, on liver fibrosis and on changes in the hepatic expressions of genes that regulate the progression of fibrosis in mice. Liver fibrosis was caused by the repetitive administration of CCl4 for 12 weeks, with ONO-1301 being administered during the last 4 weeks. The expressions of fibrogenic genes: TGF-β1, connective tissue growth factor, α-smooth muscle actin, type-I collagen, and type-III collagen were upregulated by chronic liver injury, which was associated with the expansion of myofibroblasts and the development of liver fibrosis. Treatment with ONO-1301 increased hepatic HGF mRNA expression, but decreased the expressions of TGF-β1, connective tissue growth factor, α-smooth muscle actin, and type-I and type-III collagen, which was associated with the suppression of myofibroblast expansion and liver fibrosis. Neutralizing antibody for HGF significantly attenuated the suppressive action of ONO-1301 on liver fibrosis and fibrogenic gene expressions. The therapeutic action of ONO-1301 on liver fibrosis may have occurred partly through HGF-mediated pathways. | |||||||||||
| 著者版フラグ | ||||||||||||
| 出版タイプ | VoR | |||||||||||
| 出版タイプResource | http://purl.org/coar/version/c_970fb48d4fbd8a85 | |||||||||||
