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Cilostazol attenuates ischemia?reperfusion-induced blood?brain barrier dysfunction enhanced by advanced glycation endproducts via transforming growth factor-β1 signaling
http://hdl.handle.net/10069/34603
http://hdl.handle.net/10069/346035adbdf49-20c6-40d3-9745-f4aefac9317c
| 名前 / ファイル | ライセンス | アクション |
|---|---|---|
MCN60_1.pdf (629.4 kB)
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| Item type | 学術雑誌論文 / Journal Article(1) | |||||
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| 公開日 | 2014-07-31 | |||||
| タイトル | ||||||
| タイトル | Cilostazol attenuates ischemia?reperfusion-induced blood?brain barrier dysfunction enhanced by advanced glycation endproducts via transforming growth factor-β1 signaling | |||||
| 言語 | ||||||
| 言語 | eng | |||||
| キーワード | ||||||
| 主題Scheme | Other | |||||
| 主題 | Advanced glycation endproducts | |||||
| キーワード | ||||||
| 主題Scheme | Other | |||||
| 主題 | Blood-brain barrier | |||||
| キーワード | ||||||
| 主題Scheme | Other | |||||
| 主題 | Cilostazol | |||||
| キーワード | ||||||
| 主題Scheme | Other | |||||
| 主題 | Claudin-5 | |||||
| キーワード | ||||||
| 主題Scheme | Other | |||||
| 主題 | Oxygen glucose deprivation/reoxygenation | |||||
| キーワード | ||||||
| 主題Scheme | Other | |||||
| 主題 | Transforming growth factor-β | |||||
| 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 |
Takeshita, Tomonori
× Takeshita, Tomonori× Nakagawa, Shinsuke× Tatsumi, Rie× So, Gohei× Hayashi, Kentaro× Tanaka, Kunihiko× Deli, Maria A.× Nagata, Izumi× Niwa, Masami |
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| 抄録 | ||||||
| 内容記述タイプ | Abstract | |||||
| 内容記述 | We investigated the effects of cilostazol, a selective inhibitor of phosphodiesterase 3, on blood-brain barrier (BBB) integrity against ischemia-reperfusion injury enhanced by advanced glycation endproducts (AGEs). We used in vitro BBB models with primarily cultured BBB-related cells from rats (brain capillary endothelial cells, astrocytes and pericytes), and subjected cells to either normoxia or 3-h oxygen glucose deprivation (OGD)/24-h reoxygenation with or without AGEs. Treatment of AGEs did not affect the transendothelial electrical resistance (TEER) in the BBB model under normoxia, but there was a significant decrease in TEER under 3-h OGD/24-h reoxygenation conditions with AGEs. Cilostazol inhibited decreases in TEER induced by 3-h OGD/24-h reoxygenation with AGEs. Immunocytochemical and Western blot analyses showed that AGEs reduced the expression of claudin-5, the main functional protein of tight junctions (TJs). In contrast, cilostazol increased the expression of claudin-5 under 3-h OGD/24-h reoxygenation with AGEs. Furthermore, while AGEs increased the production of extracellular transforming growth factor (TGF)-β1, cilostazol inhibited the production of extracellular TGF-β1 and restored the integrity of TJs. Thus, we found that AGEs enhanced ischemia-reperfusion injury, which mainly included decreases in the expression of proteins comprising TJs through the production of TGF-β1. Cilostazol appeared to limit ischemia-reperfusion injury with AGEs by improving the TJ proteins and inhibiting TGF-β1 signaling. | |||||
| 書誌情報 |
Molecular and Cellular Neuroscience 巻 60, p. 1-9, 発行日 2014-05 |
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| 出版者 | ||||||
| 出版者 | Academic Press Inc. | |||||
| ISSN | ||||||
| 収録物識別子タイプ | ISSN | |||||
| 収録物識別子 | 10447431 | |||||
| DOI | ||||||
| 関連タイプ | isVersionOf | |||||
| 識別子タイプ | DOI | |||||
| 関連識別子 | 10.1016/j.mcn.2014.01.006 | |||||
| 権利 | ||||||
| 権利情報 | c 2014 Elsevier Inc. | |||||
| 権利 | ||||||
| 権利情報 | NOTICE: this is the author’s version of a work that was accepted for publication in Molecular and Cellular Neuroscience. Changes resulting from the publishing process, such as peer review, editing, corrections, structural formatting, and other quality control mechanisms may not be reflected in this document. Changes may have been made to this work since it was submitted for publication. A definitive version was subsequently published in Molecular and Cellular Neuroscience, 60, (2014) | |||||
| 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 | |||||
| 引用 | ||||||
| 内容記述タイプ | Other | |||||
| 内容記述 | Molecular and Cellular Neuroscience, 60, pp.1-9; 2014 | |||||
