Sclは,予期される血源性内皮および内心臓における心筋形成を抑制する

Ben Van Handel¹, Amélie Montel-Hagen, Rajkumar Sasidharan

¹Department of Molecular, Cell, and Developmental Biology, University of California, Los Angeles, Los Angeles, CA 90095, USA.

Cell

|August 7, 2012

まとめ

転写因子Scl/Tal1は,心臓細胞ではなく,内皮細胞を血液幹細胞に指定するために重要である. その欠如により,胚内皮は意図しない心臓組織を形成し,内皮の可塑性を明らかにします.

科学分野:

発達生物学発達生物学とは
幹細胞生物学幹細胞生物学とは
心血管研究に関する研究.

背景:

胚内皮は,血造性幹細胞と祖先細胞を形成する.
内皮細胞の運命を決定する正確なメカニズムは不明である.

研究の目的:

内皮細胞の運命を決定するトランスクリプション因子Scl/Tal1の役割を調査する.
Scl/Tal1が,心臓の系統への内皮の誤指定をどのように防ぐかを理解する.

主な方法:

Scl/Tal1 ノックアウト (Scl-/-) 胚の分析
血源性内皮と黄内皮の研究.
Sclのモザイク削除は,Scl (fl/fl) Rosa26Cre-ER (T2) の胚を用いて行われます.
Wntアンタゴニストを含む遺伝子発現分析.

主要な成果:

Scl/Tal1の欠乏は,胚内皮における心臓の転写プログラムの活性化につながる.
Scl-/- 胚で観察された子宮外心形成,内皮細胞が心筋細胞に微分化.
Scl/Tal1に対する細胞内在的および時間的な要求は,内皮からの心筋形成を防ぐためです.
Scl-/-内皮におけるWntアンタゴニストのアップレギュレーションは,子宮外心筋細胞の分化を促進する.

結論:

Scl/Tal1は,血液形成プログラムを確立し,血源性内皮における心筋形成を予防するために不可欠です.
胚内皮は有意な可塑性を発揮し,Scl/Tal1の喪失により子宮外心形成が誘発される.
この研究は,Scl/Tal1が,内皮細胞の同一性を維持し,系統不忠を防止する新しい役割を明らかにしています.

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