エクソクリン細胞における局所およびグローバルな細胞溶液Ca2+振動は,アゴニストおよびイノシトール三酸塩によって誘発される

P Thorn¹, A M Lawrie, P M Smith

¹Physiological Laboratory University of Liverpool, England.

Cell

|August 27, 1993

まとめ

低濃度のアゴニストは,臓細胞の局所的なカルシウムスパイクを誘発し,液体の分泌に不可欠なイオン電流を活性化させます. これらのピークは,セルラー制御のための経済的なシグナリングメカニズムを提供します.

科学分野:

細胞生物学細胞生物学
生理学生理学とは
バイオケミストリーバイオケミストリー

背景:

アゴニスト刺激は,しばしば様々な細胞タイプにおける細胞塩酸カルシウム (Ca2+) 振動につながる.
これらのCa2+信号は,通常,プラズマ膜の近くから始まり,波として拡散します.
臓のアシナ細胞における局所的なCa2+シグナル伝達の役割については,さらなる解明が必要である.

研究の目的:

マウスの臓アシナ細胞におけるアゴニストの低,生理学的濃度によって誘発されるCa2+信号の性質を調査する.
これらのCa2+信号の起源と特性,およびIP3受容体阻害に対するその感受性を決定する.
臓機能の調節におけるこれらの局所的なCa2+イベントの生理学的重要性を理解するために.

主な方法:

単一のマウスの臓アシナ細胞にサブマキシマルアゴニスト刺激を用いた.
光画像を用いたサイトゾリックCa2+ダイナミクスのモニタリング.
細胞内イノシトール1,4,5-トリスホスファート (IP3) とIP3受容体の抗体ヘパリンを適用した.

主要な成果:

低濃度のアゴニストは,臓のアシナ細胞の分泌極に局所的な細胞性Ca2+スパイクを誘発した.
これらの局所的なピークは,IP3受容体アンタゴニストヘパリンによるブロックに敏感でした.
スパイクは,独立して,繰り返し,またはグローバルなCa2+信号に先行して発生し,細胞内IP3アプリケーションによって模倣されました.
これらのCa2+ピークは,Ca2+依存のClとカチオン電流を活性化させた.

結論:

短期的な局所的なCa2+ピークは,臓のアシナ細胞における経済的なシグナル伝達メカニズムを表しています.
これらの局所的なCa2+イベントは生理学的に重要であり,液体の分泌に不可欠なイオンチャネル活動を制御します.
この発見は,局所的なCa2+シグナル伝達が臓の外分機能の調節における特定の役割を強調しています.

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