Periostin cross‑reacts with the renin‑angiotensin system during liver fibrosis development.

• Material Type: 博士論文
• Title: Periostin cross‑reacts with the renin‑angiotensin system during liver fibrosis development.
• Author/Editor: Takeda, Kosuke; Noguchi, Ryuichi; Kitade, Mitsuteru; Namisaki, Tadashi; Moriya, Kei; Kawaratani, Hideto; Okura, Yasushi; Kaji, Kosuke; Aihara, Yosuke; Douhara, Akitoshi; Nishimura, Norihisa; Sawada, Yasuhiko; Seki, Kenichiro; Yoshiji, Hitoshi
• Author Heading: Takeda, Kosuke; Noguchi, Ryuichi; Kitade, Mitsuteru; Namisaki, Tadashi; Moriya, Kei; Kawaratani, Hideto; Okura, Yasushi; Kaji, Kosuke; Aihara, Yosuke; Douhara, Akitoshi; Nishimura, Norihisa; Sawada, Yasuhiko; Seki, Kenichiro; Yoshiji, Hitoshi
• Publication, Distribution, etc.: Spandidos Publications
• Publication Date: 2017-11
• Publication Date (W3CDTF): 2017-11
• Alternative Title: 肝線維化におけるペリオスチンの役割 : レニン・アンギオテンシン系とクロストーク
• Periodical title: Molecular medicine reports
• No. or year of volume/issue: 16 5
• Volume: 16
• Issue: 5
• Pages: 5752-5758
• ISSN (Periodical Title): ISSN : 1791-2997
• Degree grantor/type: 奈良県立医科大学
• Date Granted: 2018-03-15
• Dissertation Number: 乙第1413号
• Degree Type: 博士（医学）
• Text Language Code: eng
• Subject Heading: periostin; angiotensin II; liver fibrosis; renin-angiotensin system; choline-supplemented amino acid
• Target Audience: 一般
• Note (General): type:Thesis; Periostin is a 90‑kDa extracellular matrix protein, which is secreted primarily from fibroblasts and is expressed in the lungs, kidneys and heart valves. Angiotensin II (AT‑II) serves pivotal roles in the pathogenesis of several diseases with accompanying fibrosis, including chronic liver diseases. AT‑II induces periostin expression by regulating transforming growth factor‑β1 (TGF‑β1)/Smad signaling during cardiac fibrosis. The aim of the present study was to investigate the interaction between AT‑II and periostin during liver fibrosis development. Fischer 344 rats were fed a choline‑deficient L‑amino‑acid (CDAA)‑defined diet for 12 weeks to simulate the development of steatohepatitis with liver fibrosis. Losartan, an AT‑II type I receptor blocker, was administered to inhibit the effect of AT‑II. The therapeutic effect of losartan on hepatic fibrosis development and on periostin expression was then evaluated. Several in vitro experiments were performed to examine the mechanisms underlying the interaction between AT‑II and periostin in activated hepatic stellate cells (Ac‑HSCs). Treatment with losartan suppressed the development of liver fibrosis induced by the CDAA diet, and reduced hepatic periostin expression. In addition, losartan treatment suppressed hepatic Ac‑HSC expansion and hepatic TGF‑β1 expression. In vitro analysis using LX2 HSC cells indicated that AT‑II can augment TGF‑β1 and collagen type I α1 mRNA expression via periostin expression, suggesting that the interaction between AT‑II and periostin may serve a role in liver fibrosis development. In conclusion, blockade of AT‑II‑induced periostin may suppress the progression of liver fibrosis development.; 博士（医学）・乙第1413号・平成30年3月15日; Copyright: © Takeda et al. This is an open access article distributed under the terms of Creative Commons Attribution License(CC BY-NC-ND 4.0) https://creativecommons.org/licenses/by-nc-nd/4.0/.; identifier:Molecular medicine reports Vol.16 No.5 p.5752-5758 (2017 Nov); identifier:17912997; identifier:http://ginmu.naramed-u.ac.jp/dspace/handle/10564/3429; identifier:Molecular medicine reports, 16(5): 5752-5758
• Source: fulltext; http://ginmu.naramed-u.ac.jp/dspace/bitstream/10564/3429/1/01%e4%b9%991413%e6%9c%ac%e6%96%87%e3%81%ae%e8%a6%81%e6%97%a8.pdf; http://ginmu.naramed-u.ac.jp/dspace/bitstream/10564/3429/2/02%e4%b9%991413%e5%af%a9%e6%9f%bb%e8%a6%81%e6%97%a8.pdf; http://ginmu.naramed-u.ac.jp/dspace/bitstream/10564/3429/3/03%e4%b9%991413%e6%9c%ac%e6%96%87.pdf
• Access Restrictions: インターネット公開
• Related Material (DOI): 10.3892/mmr.2017.7356
• Data Provider (Database): 国立情報学研究所 : 学術機関リポジトリデータベース（IRDB）（機関リポジトリ）; https://irdb.nii.ac.jp
• Original Data Provider (Database): 奈良県立医科大学 : 奈良県立医科大学機関リポジトリ GINMU