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  1. Public
  2. 研究紀要
  3. Acta Medica Kindai University
  4. 43(1)2018

<Original> Atorvastatin promoted in vitro angiogenesis by reduction of geranylgeranyl pyrophosphate in a dose-dependent manner and protected against rho kinase-mediated endothelial cell damage caused by thromboxane A2

https://kindai.repo.nii.ac.jp/records/19497
https://kindai.repo.nii.ac.jp/records/19497
4ac30f6e-809b-42d7-b11b-ec26a4516154
名前 / ファイル ライセンス アクション
AA0050842X-20180600-0035.pdf AA0050842X-20180600-0035.pdf (713.7 kB)
Item type ☆紀要論文 / Departmental Bulletin Paper(1)
公開日 2018-07-26
タイトル
タイトル <Original> Atorvastatin promoted in vitro angiogenesis by reduction of geranylgeranyl pyrophosphate in a dose-dependent manner and protected against rho kinase-mediated endothelial cell damage caused by thromboxane A2
言語 en
著者 Yokota, Ryoji

× Yokota, Ryoji

Yokota, Ryoji

ja-Kana ヨコタ, リョウジ

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Nishi, Yuko

× Nishi, Yuko

Nishi, Yuko

ja-Kana ニシ, ユウコ

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Sugitani, Yuuki

× Sugitani, Yuuki

Sugitani, Yuuki

ja-Kana スギタニ, ユウキ

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Tamada, Hiroyuki

× Tamada, Hiroyuki

Tamada, Hiroyuki

ja-Kana タマダ, ヒロユキ

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Ohi, Yohei

× Ohi, Yohei

Ohi, Yohei

ja-Kana オオイ, ヨウヘイ

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Ishikawa, Chisato

× Ishikawa, Chisato

Ishikawa, Chisato

ja-Kana イシカワ, チサト

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Ohe, Kentarou

× Ohe, Kentarou

Ohe, Kentarou

ja-Kana オオエ, ケンタロウ

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Uemori, Noritsugu

× Uemori, Noritsugu

Uemori, Noritsugu

ja-Kana ウエモリ, ノリツグ

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Mitsuoka, Hirokazu

× Mitsuoka, Hirokazu

Mitsuoka, Hirokazu

ja-Kana ミツオカ, ヒロカズ

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Togi, Kiyonori

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Togi, Kiyonori

ja-Kana トギ, キヨノリ

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Shirotani, Manabu

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Shirotani, Manabu

ja-Kana シロタニ, マナブ

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言語
言語 eng
キーワード
主題 Angiogenesis, Endothelial cells, Statin, Geranylgeranyl pyrophosphate, Rho kinase, Thromboxane A2, Caspase-3
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 departmental bulletin paper
著者 所属
値 Cardiovascular Center, Nara Hospital, Kindai University Faculty of Medicine
著者 所属
値 Cardiovascular Center, Nara Hospital, Kindai University Faculty of Medicine
著者 所属
値 Cardiovascular Center, Nara Hospital, Kindai University Faculty of Medicine
著者 所属
値 Cardiovascular Center, Nara Hospital, Kindai University Faculty of Medicine
著者 所属
値 Cardiovascular Center, Nara Hospital, Kindai University Faculty of Medicine
著者 所属
値 Cardiovascular Center, Nara Hospital, Kindai University Faculty of Medicine
著者 所属
値 Cardiovascular Center, Nara Hospital, Kindai University Faculty of Medicine
著者 所属
値 Cardiovascular Center, Nara Hospital, Kindai University Faculty of Medicine
著者 所属
値 Cardiovascular Center, Nara Hospital, Kindai University Faculty of Medicine
著者 所属
値 Cardiovascular Center, Nara Hospital, Kindai University Faculty of Medicine
著者 所属
値 Cardiovascular Center, Nara Hospital, Kindai University Faculty of Medicine
版
出版タイプ NA
出版タイプResource http://purl.org/coar/version/c_be7fb7dd8ff6fe43
出版者 名前
出版者 Kindai University Medical Association
書誌情報 en : ACTA MEDICA KINDAI UNIVERSITY

巻 43, 号 1, p. 35-42, 発行日 2018-06
ISSN
収録物識別子タイプ ISSN
収録物識別子 03866092
抄録
内容記述タイプ Abstract
内容記述 [Abstract] Background: Atorvastatin can inactivate Rho/Rho kinase via a reduction in the synthesis of geranylgeranyl pyrophosphate (GGPP).Thromboxane A2 (TxA2) causes endothelial cell (EC) apoptosis via Rho/Rho kinase activation.We tested the hypothesis that atorvastatin protects against the Rho kinase-mediated anti-angiogenic effect of TxA2. Methods: We used human coronary artery ECs to form tubular structures on plates coated with a basement membrane matrix gel. The number of tubular structure was counted under a microscope. The caspase-3 activity was used as a determinant of apoptosis.Results: Atorvastatin significantly increased the number of tubes in a dose-dependent manner, and this effect was blocked by mevalonate or geranylgeranyl pyrophosphate (GGPP). Similar to atorvastatin, a potent selective inhibitor of geranylgeranyl transferase type I enhanced tubular formation. A TxA2 mimetic (IBOP) inhibited formation of EC tubular structures. The inhibitory effect was completely blocked by a TxA2 antagonist (SQ29548), a Rho kinase inhibitor (Y27632), and by atorvastatin. The IBOP-induced increase in caspase-3 activity was attenuated by atorvastatin. Conclusions: Atorvastatin promoted in vitro angiogenesis of ECs in a dose-dependent manner and reversed the TxA2 receptor-mediated antiangiogenic effect. We suggest that reduction of GGPP and inactivation of Rho kinase plays an important role in the proangiogenic effect of atorvastatin.
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内容記述 application/pdf
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