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  1. H-1. がん進展制御研究所
  2. h-1 10. 学術雑誌掲載論文
  3. 1. 査読済論文

Suppression of fibrogenic gene expression and liver fibrosis using a synthetic prostacyclin agonist

https://doi.org/10.24517/00027524
https://doi.org/10.24517/00027524
e61e346d-7854-4c16-8f99-8482b50f69d5
名前 / ファイル ライセンス アクション
CA-PR-MATSUMOTO-K-241.pdf CA-PR-MATSUMOTO-K-241.pdf (1.7 MB)
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Item type 学術雑誌論文 / Journal Article(1)
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 10.24517/00027524
ID登録タイプ JaLC
著者 Xu, Qing

× Xu, Qing

WEKO 48019

Xu, Qing

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Sakai, Katsuya

× Sakai, Katsuya

WEKO 88142
e-Rad 10523318

Sakai, Katsuya

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Suzuki, Yoshinori

× Suzuki, Yoshinori

WEKO 47514

Suzuki, Yoshinori

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Tambo, Chikako

× Tambo, Chikako

WEKO 47611

Tambo, Chikako

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Sakai, Yoshiki

× Sakai, Yoshiki

WEKO 48022

Sakai, Yoshiki

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松本, 邦夫

× 松本, 邦夫

WEKO 27
e-Rad 90201780
金沢大学研究者情報 90201780
研究者番号 90201780

ja ISNI

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著者別表示 酒井, 克也

× 酒井, 克也

酒井, 克也

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松本, 邦夫

× 松本, 邦夫

ja ISNI

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書誌情報 Biomedical Research (Japan)

巻 34, 号 5, p. 241-250, 発行日 2013-01-01
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
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