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VE-カデリン/ベータ-カテニンの発現障害は,拡張性心筋疾患における内皮細胞変性を媒介する
Romana Schäfer1, Dietmar Abraham, Patrick Paulus
1Laboratory for Cardiovascular Research, Department of Anatomy, University of Vienna, Vienna, Austria.
Circulation
|September 10, 2003
まとめ
拡張性心筋症 (DCM) では,VEGFから独立して減少したVE-cadherin/β-cateninにより,内皮細胞生存率が低下します. VE-カデリンをターゲットにすることで,DCMに関連するEC病理を治療することができます.
科学分野:
- 心血管生物学 心血管生物学
- 細胞生物学 細胞生物学
- 分子医学は分子医学である.
背景:
- 血管内皮成長因子 (VEGF) -A,アンジオポエチン (Ang),およびVE-カデリン相互作用は,内皮細胞 (EC) の生存を調節する.
- 心臓のVEGF-A発現は拡張性心筋病変 (DCM) で減少しますが,VE-cadherin/Ang信号伝達の役割は不明です.
研究 の 目的:
- DCM患者の心筋内におけるVE-cadherin/β-cateninおよびangiopoietinシグナル伝達の機能を調査する.
- DCMにおけるVE-cadherin/β-catenin,アンジオポエチン,および内皮細胞変性との関係を決定する.
主な方法:
- DCM,発血性心筋症 (ICM),およびリアルタイムRT-PCR,ウエスタン・ブロッティング,および免疫細胞化学を用いた対照被験者におけるVE-カデリン/ベータ-カタニン,Ang-1,Ang-2,およびTie-2の心筋表情を調べた.
- 伝送電子顕微鏡 (TEM) による定量化された内皮細胞変性.
- 培養細胞におけるRNA干渉とVEGF操作を利用して,分子相互作用を探求した.
主要な成果:
- VE-cadherin/β-cateninの発現は,DCMでは著しくダウンレギュレーションされたが,ICMではそうではなかった.
- Ang-2発現はDCMとICMの両方でダウンレギュレーションされ,Tie-2タンパク質はアップレギュレーションされた.
- DCMではICMと比較して内皮細胞の変性率が高く,VE-cadherin遺伝子の静止はDCMに関連するEC病理を模倣した.
結論:
- DCMでは内皮細胞生存が低下し,VE-cadherin/β-catenin機能不全に関連しており,おそらくVEGFから独立している.
- VE-カデリンをターゲットにすることは,DCMに関連した内皮細胞病理学の潜在的な治療戦略です.
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