COUP-TFII転写因子によるノッチ信号の抑制は,静脈の同一性を調節する
Li-Ru You1, Fu-Jung Lin, Christopher T Lee
1Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, Texas 77030, USA.
Nature
|May 6, 2005
まとめ
血管内皮成長因子 (VEGF) 信号伝達は,血管のアイデンティティを調節する. COUP-TFIIタンパク質は,Notchシグナリングを抑制し,静脈発達の遺伝的コントロールを明らかにすることによって,静脈のアイデンティティを維持するために重要である.
科学分野:
- 心血管生物学 心血管生物学
- 分子生物学は分子生物学である.
- 発達生物学 発達生物学とは
背景:
- 動脈と静脈は,異なる解剖学的,機能的,分子的な特性を有する.
- 現在のモデルでは,血管内皮成長因子 (VEGF) とノッチ信号が動脈の同一性に関係しているが,静脈の同一性規制は不明である.
研究 の 目的:
- 静脈のアイデンティティを調節する分子機構を調査する.
- 血管系における内皮細胞の運命を左右する重要なレギュレータを特定する.
主な方法:
- マウス胚の内皮細胞におけるCOUP-TFII (Nr2f2) 発現の分析.
- 内皮細胞におけるCOUP-TFIIの条件付きノックアウト.
- トランス遺伝子マウスにおける動脈・静脈マーカー発現と血管形態の評価.
主要な成果:
- COUP-TFIIは特に静脈内皮で表現される.
- 内皮細胞におけるCOUP-TFIIの喪失により,静脈は神経ピリン1 (NP-1) とノッチ信号伝達を含む動脈特性を獲得する.
- 子宮外COUP-TFII発現はネズミの胚で動脈静脈融合を引き起こす.
結論:
- COUP-TFIIは,静脈の同一性を維持するためにノッチ信号を抑制する上で重要な役割を果たします.
- 静脈のアイデンティティは遺伝的に制御され,デフォルトの経路ではありません.
- COUP-TFIIは,血管のアイデンティティの重要な決定因子です.
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