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内生性エンドセリン-1は,体内での心筋細胞生存のために必要である

Xiao-Song Zhao¹, Wentong Pan, Raffi Bekeredjian

¹Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas, USA.

|August 16, 2006

まとめ

心臓細胞におけるエンドセリン-1 (ET-1) 欠失は,老齢マウスの腹筋拡張症と心不全を引き起こす. これは,アポトーシスの増加とNF-kappaBシグナル伝達の減少によるもので,ET-1の保護的役割を強調しています.

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
遺伝子モデル遺伝子モデル

背景:

エンドオセリン-1 (ET-1) は,強力な血管収縮剤であり,過剰縮小因子である.
ET-1受容体アンタゴニストは,肺高血圧に使用され,心不全のために調査されています.
心臓機能における内生性ET-1の役割は不明でした.

研究の目的:

心臓機能の維持における心筋細胞由来ET-1の役割を調査する.
ET-1欠乏が心臓の構造とストレス下での生存に与える影響を決定する.

主な方法:

心筋細胞特異的なET-1のデリレーションを持つマウスを生成した.
エコカルジオグラフィーとヒストロジーを用いて心臓機能を評価した.
アポトーシス,TNFシグナル伝達,NF-kappaB活性について分析した.

主要な成果:

心筋細胞ET-1の消去は,若いマウスの正常な表型につながったが,老化や圧力過負荷による漸進的な拡張性心筋病症につながった.
ET-1欠乏性の心臓は,アポトーシスの増加とTNF媒介の細胞死亡の増大を示した.
NF-kappaBの活性低下が観察され,TNFシグナル伝達の抑制が低下しました.

結論:

地元のET-1遺伝子発現は,心臓機能と心筋細胞の生存を維持するために不可欠です.
ET-1は,NF-kappaBシグナル伝達を通じてTNF関連のアポトーシスを調節することによって心臓を保護する.
この研究では,心臓における内生性ET-1に対する新しい保護的役割が明らかになりました.

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