Mechanisms Underlying Activation of α1-Adrenergic Receptor-Induced Trafficking of AQP5 in Rat Parotid Acinar Cells under Isotonic or Hypotonic Conditions

• 資料種別: 博士論文
• ISSN: 1422-0067
• タイトル: Mechanisms Underlying Activation of α1-Adrenergic Receptor-Induced Trafficking of AQP5 in Rat Parotid Acinar Cells under Isotonic or Hypotonic Conditions
• 巻次・部編番号: 17 7
• 著者・編者: Bragiel, Aneta Magdalena; Wang, Di; Pieczonka, Tomasz D.; Shono, Masayuki; Ishikawa, Yasuko
• 著者標目: Bragiel, Aneta Magdalena; Wang, Di; Pieczonka, Tomasz D.; Shono, Masayuki; Ishikawa, Yasuko
• 出版事項: MDPI
• 出版年月日等: 2016-06-28
• 出版年（W3CDTF）: 2016-06-28
• 並列タイトル等: 等張または低張条件下のラット耳下腺腺房細胞におけるα１-アドレナリン受容体誘導性のAQP5細胞内移動機序
• タイトル（掲載誌）: International Journal of Molecular Sciences
• 授与機関名: 徳島大学
• 授与年月日: 2017-03-23
• 授与年月日（W3CDTF）: 2017-03-23
• 報告番号: 甲第3071号
• 学位: 博士（学術）
• 博論授与番号: 甲第3071号
• 本文の言語コード: eng
• 件名標目: aquaporin-5; α1A-adrenoceptor; α1B-adrenoceptor; α1D-adrenoceptor; calcium; protein G kinase; hypotonicity
• 対象利用者: 一般
• 一般注記: Defective cellular trafficking of aquaporin-5 (AQP5) to the apical plasma membrane (APM) in salivary glands is associated with the loss of salivary fluid secretion. To examine mechanisms of α1-adrenoceptor (AR)-induced trafficking of AQP5, immunoconfocal microscopy and Western blot analysis were used to analyze AQP5 localization in parotid tissues stimulated with phenylephrine under different osmolality. Phenylephrine-induced trafficking of AQP5 to the APM and lateral plasma membrane (LPM) was mediated via the α1A-AR subtype, but not the α1B- and α1D-AR subtypes. Phenylephrine-induced trafficking of AQP5 was inhibited by ODQ and KT5823, inhibitors of nitric oxide (NO)-stimulated guanylcyclase (GC) and protein kinase (PK) G, respectively, indicating the involvement of the NO/ soluble (c) GC/PKG signaling pathway. Under isotonic conditions, phenylephrine-induced trafficking was inhibited by La3+, implying the participation of store-operated Ca2+ channel. Under hypotonic conditions, phenylephrine-induced trafficking of AQP5 to the APM was higher than that under isotonic conditions. Under non-stimulated conditions, hypotonicity-induced trafficking of AQP5 to the APM was inhibited by ruthenium red and La3+, suggesting the involvement of extracellular Ca2+ entry. Thus, α1A-AR activation induced the trafficking of AQP5 to the APM and LPM via the Ca2+/ cyclic guanosine monophosphate (cGMP)/PKG signaling pathway, which is associated with store-operated Ca2+ entry.
• DOI: info:doi/10.3390/ijms17071022; https://doi.org/info:doi/10.3390/ijms17071022
• 国立国会図書館永続的識別子: info:ndljp/pid/10993560; https://dl.ndl.go.jp/pid/10993560
• コレクション（共通）: 障害者向け資料
• コレクション（障害者向け資料：レベル1）: テキストデータ
• コレクション（個別）: 国立国会図書館デジタルコレクション > デジタル化資料 > 博士論文; https://dl.ndl.go.jp/collections/A00014
• 収集根拠: 博士論文（自動収集）
• 受理日（W3CDTF）: 2017-12-04T02:02:48+09:00
• 記録形式（IMT）: application/pdf
• オンライン閲覧公開範囲: 国立国会図書館内限定公開
• デジタル化資料送信: 図書館・個人送信対象外
• 遠隔複写可否（NDL）: 可
• 掲載誌（URI）: http://repo.lib.tokushima-u.ac.jp/112395
• 連携機関・データベース: 国立国会図書館 : 国立国会図書館デジタルコレクション; https://dl.ndl.go.jp

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2019-09-09 再収集