内皮のシリアは,ポリシスティン-1を介してカルシウムシグナル伝達と酸化窒素生成を調節する流体剪定センサーです
Surya M Nauli1, Yoshifumi Kawanabe, John J Kaminski
1Department of Pharmacology and Medicine, College of Pharmacy and Medicine, University of Toledo, Toledo, Ohio 43606, USA. Surya.Nauli@UToledo.edu
Circulation
|February 21, 2008
まとめ
内皮細胞は,ポリシスティン-1の局所化に不可欠なシリアを使用して,流体切断ストレスを感知します. このメカニズムは,酸化窒素の放出と細胞の通信に不可欠です.
科学分野:
- 細胞生物学 細胞生物学
- 機械生物学のメカノバイオロジー
- 血管生物学 血管生物学とは
背景:
- 血管内皮細胞は,流体切断ストレスに反応して酸化窒素を放出します.
- シリア,アピカル膜の臓器細胞は,内皮細胞が低レベルの流体切断ストレスを感知するために不可欠です.
- シリアは,機械感受性ポリシスティン-1分子の正しい局所化と機能のために必要です.
研究 の 目的:
- 内皮細胞の機械伝導におけるシリアとポリシスティン-1の役割を調査する.
- 内皮細胞が細胞外流体の切断ストレスを感知し,それに反応する方法を決定する.
主な方法:
- Pkd1 (ポリシスティン-1をコードする) とTg737 (ポラリスをコードする) の変異を有する内皮細胞を使用した.
- 流体切断ストレスに反応した細胞内カルシウムシグナル伝達と酸化窒素合成の測定.
- 切断ストレスレベルによって異なるポリシスティン-1の局所性を調べました.
主要な成果:
- Pkd1 ((null/null) とTg737 ((orpk/orpk) の変異細胞は,切断ストレスをカルシウムシグナル伝達と酸化窒素生成に伝達できませんでした.
- 流体シーアセンシングは,他の刺激が変異細胞のシグナル伝達に影響を与えないため,シリア特有のメカニズムです.
- 基礎体内のポリシスティン-1は剪定ストレス反応には不十分であり,最適の剪定ストレスがタンパク質分解によってポリシスティン-1を改変した.
結論:
- ポリシスティン-1とポラリスは,内皮細胞における不可欠な機械感受性分子であり,ポリシスティン-1は乳毛の機能に,ポラリスは乳毛の構造に不可欠である.
- シリア内のポリシスティン-1の適切な局所化と機能は,細胞外マイクロ環境との内皮細胞の通信に不可欠です.
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