原始的および最終的な血液形成および血管新生における Flk1 の要件である

F Shalaby¹, J Ho, W L Stanford

¹Samuel Lunenfeld Research Institute, Mount Sinai Hospital, Toronto, Ontario, Canada.

Cell

|June 13, 1997

まとめ

Flk1受容体チロシンキナーゼは,マウスの内皮細胞発育と血液形成に不可欠です. Flk1の欠乏は,細胞が血液の島を形成するのを妨げ,血管新生と血液形成の両方に影響を及ぼします.

科学分野:

発達生物学発達生物学とは
ヘマトポエーシス (血液形成) とは
内皮細胞生物学エンドセル細胞生物学

背景:

受容体チロシンキナーゼは,細胞のシグナル伝達と発達において重要な役割を果たします.
Flk1 (VEGFR2) は,早期の血液と血管形成に関与する重要な受容体です.

研究の目的:

血管新生と血液形成の間に胚性幹細胞におけるFlk1の細胞自律的な役割を調査する.
Flk1欠乏細胞が血液の島形成と血液形成の発達に与える貢献を決定する.

主な方法:

Flk1-/- 胚性幹細胞を用いたキメリック胚の生成.
キメリックの黄袋,胎児の肝臓,成人マウスの内皮細胞と血球細胞の発達を分析した.

主要な成果:

Flk1は,内皮の発達に細胞自律的に必要である.
Flk1-/-細胞は,原始的および決定的な血液形成に寄与できませんでした.
Flk1欠乏症は,細胞の移動を後部原始線状と黄袋に阻害し,血の島形成を妨げました.

結論:

Flk1シグナル伝達は,内皮細胞の発達に不可欠である.
Flk1は,血液形成の原始細胞の移動と分化に不可欠です.
この研究は,初期胚形成における内皮系と血液系の両方におけるFlk1の二重の役割を強調しています.

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