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Localization of Xenobiotic Transporter OCTN1/SLC22A4 in Hepatic Stellate Cells and Its Protective Role in Liver Fibrosis
http://hdl.handle.net/2297/45429
http://hdl.handle.net/2297/45429548b9181-6fa9-4d15-8f72-5ec50dd767dd
| 名前 / ファイル | ライセンス | アクション |
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PH-PR-KATO-Y-1779.pdf (278.4 kB)
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| Item type | 学術雑誌論文 / Journal Article(1) | |||||
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| 公開日 | 2017-10-04 | |||||
| タイトル | ||||||
| タイトル | Localization of Xenobiotic Transporter OCTN1/SLC22A4 in Hepatic Stellate Cells and Its Protective Role in Liver Fibrosis | |||||
| 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 |
Tang, Yaliang
× Tang, Yaliang× Masuo, Yusuke× Sakai, Yoshio× Wakayama, Tomohiko× Sugiura, Tomoko× Harada, Ryuichi× Futatsugi, Azusa× Komura, Takuya× Nakamichi, Noritaka× Sekiguchi, Hirotaka× Sutoh, Keita× Usumi, Koji× Iseki, Shoichi× Kaneko, Shuichi× Kato, Yukio |
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| 書誌情報 |
Journal of Pharmaceutical Sciences 巻 105, 号 5, p. 1779-1789, 発行日 2016-05-01 |
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| ISSN | ||||||
| 収録物識別子タイプ | ISSN | |||||
| 収録物識別子 | 0022-3549 | |||||
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| 収録物識別子タイプ | NCID | |||||
| 収録物識別子 | AA00704450 | |||||
| DOI | ||||||
| 関連タイプ | isVersionOf | |||||
| 識別子タイプ | DOI | |||||
| 関連識別子 | 10.1016/j.xphs.2016.02.023 | |||||
| 出版者 | ||||||
| 出版者 | American Pharmacists Association / Elsevier | |||||
| 抄録 | ||||||
| 内容記述タイプ | Abstract | |||||
| 内容記述 | Xenobiotic transporters play key roles in disposition of certain therapeutic agents, although limited information is available on their roles other than pharmacokinetic issues. Here, suppressive effect of multispecific organic cation transporter OCTN1/SLC22A4 on liver fibrosis was proposed in liver injury models. After injection of hepatotoxins such as dimethylnitrosamine (DMN) or concanavalin A, hepatic fibrosis, and oxidative stress, evaluated in terms of Sirius red and 4-hydroxy-2-nonenal staining, respectively, were more severe in liver of octn1/slc22a4 gene knockout (octn1-/-) mice than that in wild-type mice. DMN treatment markedly increased α-smooth muscle actin and F4/80, markers of activated stellate and Kupffer cells, respectively, in liver of octn1-/-, but had less effect in wild-type mice. Thus, octn1/slc22a4 gene deletion results in more severe hepatic fibrosis, oxidative stress, and inflammation. DMN-treated wild-type mice showed increased Octn1 staining and hepatic concentration of its food-derived antioxidant ergothioneine (ERGO). The upregulated Octn1 was co-localized with α-smooth muscle actin. Functional expression of Octn1 was demonstrated in activated human hepatic stellate cell lines, LI90 and LX-2. Provision of ERGO-rich feed ameliorated DMN-induced liver fibrosis and oxidative stress. Overall, Octn1 is upregulated in activated stellate cells, resulting in increased delivery of its substrate antioxidant ERGO and a protective effect against liver fibrosis. © 2016 American Pharmacists Association. Published by Elsevier Inc. All rights reserved. | |||||
| 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 © American Pharmacists Association / 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 | |||||
| 関連URI | ||||||
| 識別子タイプ | URI | |||||
| 関連識別子 | http://www.elsevier.com/locate/issn/00223549 | |||||
