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プロテアゼ活性化受容体-1は,心臓の改造と高縮に寄与する

Rafal Pawlinski¹, Michael Tencati, Craig R Hampton

¹The Scripps Research Institute, Department of Immunology, 10550 N Torrey Pines Rd, La Jolla, CA 92037, USA.

|October 31, 2007

まとめ

プロテアゼ活性化受容体-1 (PAR-1) 欠乏症は,左心室の膨張を減少させることで,心損傷後の心臓機能を改善します. しかし,PAR-1欠乏は心臓発作の大きさに影響を及ぼさなかったが,過剰発現は特異的縮を誘発した.

科学分野:

心血管生物学心血管生物学
分子心臓病学分子心臓病学
トロンボシス研究研究

背景:

プロテアゼ活性化受容体-1 (PAR-1) は,トロンビンの受容体であり,心筋細胞や線維芽細胞などの心臓細胞で発現する.
PAR-1シグナル伝達は,心筋細胞増殖と線維細胞増殖に関与しています.
組織因子 (TF) とトロンビンは,心不全-再注射 (I/R) 損傷への貢献因子として知られています.

研究の目的:

心筋梗塞,再構成,およびI/R損傷後の高縮におけるPAR-1の役割を調査する.
心筋細胞特異のPAR-1過剰発現が心臓の機能と構造に与える影響を分析する.

主な方法:

PAR-1欠乏症 (PAR-1-/-) と心臓のI/R損傷を受けた野生型のマウスを利用した.
心臓の再構築と機能をエコーカルディオグラフィと組織学的分析を用いて調査した.
心筋細胞特異のPAR-1過剰発現とTF遺伝子消去の影響を調査した.

主要な成果:

PAR-1欠乏症は,左心房の膨張を弱め,I/R損傷から2週間後に心臓の機能を改善しました.
PAR-1欠乏症は心臓発作の大きさを変化させなかったが,損傷した領域におけるERK1/2の活性化を増加させた.
心筋細胞特異的なPAR-1過剰発現は,心筋細胞のTF遺伝子を削除することによって減少した,特異的高縮と拡張心筋病を引き起こした.

結論:

PAR-1は,心筋梗塞後の心臓の改造と高縮において重要な役割を果たします.
カーディオミオサイトにおけるPAR-1の過剰発現は,エキセントリック・ハイパートロフィーを誘発し,膨張性心筋症のメカニズムを示唆する.
PAR-1を標的にすることは,心筋梗塞後の心筋縮および心不全を減らすための新しい治療戦略を提供することができる.

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