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中性粒子の由来マトリックスメタルプロテアゼ9は急性大動脈解剖を誘発する

Tomohiro Kurihara¹, Ryoko Shimizu-Hirota, Masayuki Shimoda

¹Department of Emergency and Critical Care Medicine, School of Medicine, Keio University, Tokyo, Japan

|November 9, 2012

まとめ

急性大動脈解剖 (AAD) は,アンジオテンシンIIに対する反応として,中性粒子がマトリックスメタルプロテインーゼ-9 (MMP9) を放出することを含む. MMP9を阻害したり中性粒子を減少させたりすると,AADの発生率が著しく低下します.

科学分野:

心血管生物学心血管生物学
血管病理学血管病理学
マトリックス生物学 (Matrix Biology) とは

背景:

急性大動脈解剖 (AAD) は,効果的な薬剤による治療法がない重大な状態です.
マトリックス金属タンパク質酵素 (MMPs) は血管疾患に関与しているが,AADにおける特定の役割は不明である.

研究の目的:

AADの病原性におけるMMPの役割を調査する.
AADを駆動する主要な分子効果因子とメカニズムを特定する.

主な方法:

AAD患者の循環中のMMPをスクリーニングした.
血管新生二酸化酵素注入とリシル酸化酵素阻害剤を使用してAADのための新しいマウスモデルを開発しました.
マウスモデルで投与されたMMP阻害剤と抗中性粒子の抗体.

主要な成果:

AAD患者におけるMMP9およびアンジオテンシンII値上昇.
高い発生率のマウスモデルでAADを成功裏に誘導した.
MMP9の過剰発現と中性粒子の浸透は,解剖された大動脈で観察されました.
MMP阻害と中性粒子の減少は,AADの発生率を著しく減少させた.

結論:

大動脈内膜に浸透した中性粒子は,アンジオテンシンIIへの反応としてMMP9を放出し,AADを誘発する.
MMP9は,初期の中性粒子の浸透レベルとは関係なく,AADの発達において重要な役割を果たします.

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