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誘導受容体プレキシンD1は,内皮細胞内のメカノセンサである

Vedanta Mehta^1,2, Kar-Lai Pang^1,2, Daniel Rozbesky^2,3

¹Cardiovascular Medicine, Radcliffe Department of Medicine, University of Oxford, Oxford, UK.

|February 7, 2020

まとめ

Plexin D1 (PLXND1) は,内皮細胞における新しいメカノセンサとして作用し,血流切断のストレスを検出します. この発見により動脈硬化症を含む心血管疾患を制御する新しいメカニズムが明らかになりました

科学分野:

心血管生物学
機械生物学
細胞シグナリング

背景:

血流によるシェアストレスは,動脈硬化を含む血管の健康と病気に影響します.
内皮細胞は分子メカノセンサを使用して切断ストレスを解釈し,アテロプロテクティブまたはアテロゲン的な結果を導きます.
細胞誘導として知られるプレキシンは,メカニカル伝達におけるその役割について以前は調査されていませんでした.

研究の目的:

内皮細胞のメカノセンセーションにおけるプレキシンD1 (PLXND1) の役割と,機械的に誘発された心血管疾患への関与を調査する.
PLXND1が血管系における直接切断ストレスのセンサーとして機能するかどうかを判断する.
PLXND1がシェア・ストレスの反応を媒介する分子メカニズムを解明する.

主な方法:

内皮細胞を用いた in vitro および in vivo 研究
切断ストレスに対する PLXND1 の役割の分析.
ニューロピリン-1とVEGFR2によるPLXND1複合体の形成の調査
PLXND1の分子構造を調べた

主要な成果:

プレキシンD1 (PLXND1) は,体内および体内の両方で,切断ストレスに対する内皮細胞の反応に不可欠です.
PLXND1は動脈硬化病変の局所化を調節する.
PLXND1は機械的な力を直接感知し,結合複合体とインテグリンより上流にある神経ピリン-1とVEGFR2とメカノ複合体を形成する.
PLXND1は,異なる分子構成を通して,リガンドまたは力受容体としてバイナリ機能を発揮する.

結論:

プラキシンD1 (PLXND1) は,心臓血管病理学にとって重要な内皮細胞における新しいメカニセンサとして特定されています.
PLXND1は内皮細胞の機敏性を媒介し,動脈硬化症の発生に影響する.
単一の受容体であるPLXND1は,機械的刺激に対する多様な細胞反応を媒介するために,異なる分子構造を通して機能することができる.

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