ニューラル幹細胞の栄養反応性グリア制御は静止状態から離脱する
James M Chell1, Andrea H Brand
1The Gurdon Institute and Department of Physiology, Development, and Neuroscience, University of Cambridge, Tennis Court Road, Cambridge CB2 1QN, UK.
Cell
|December 25, 2010
まとめ
栄養は,膠質細胞にインスリンのようなペプチドを生成する信号を送り,ドロソフィラの静止中の神経幹細胞 (ニューロブラスト) を再活性化させます. この経路は,全身のコントロールを回避し,食事中のタンパク質なしで成長を可能にします.
科学分野:
- 発達生物学 発達生物学とは
- 幹細胞の調節について
- 神経科学は神経科学である.
背景:
- 系統的調節は,幹細胞の静止と増殖を制御し,生物のニーズを満たします.
- ドロソフィラのニューロブラストは,栄養に依存する信号によって調節される,発達中の静止期を示します.
- ニューロブラストの静止状態からの脱出の正確な経路は,ほとんど不明のままです.
研究 の 目的:
- ドロソフィラニューロブラストの静止状態を調節する栄養に依存する経路を特定するために.
- ニューロブラスト再活性化におけるインスリン/IGF類ペプチドの役割を明らかにする.
- 系統信号が幹細胞の運命をどのように制御するかを理解する.
主な方法:
- 発達中のドロソフィラの神経芽細胞の行動を調査した.
- インスリン/IGFのようなペプチドを生成する,特定された膠質細胞.
- インスリン/IGFのようなペプチドの発現とPI3K/Aktのシグナル伝達を変更するために遺伝子操作を使用した.
主要な成果:
- 栄養に反応してインスリン/IGFのようなペプチドを生成する膠質細胞を発見した.
- ニューロブラスト静止退出のためのインスリン/IGF受容体経路の必要性を実証した.
- 強制的なインスリン/IGF型ペプチド発現またはPI3K/Aktの活性化が,食事中のタンパク質とは無関係に増殖を誘発することを示した.
結論:
- グリアル系インスリン/IGF型ペプチドは,栄養依存性ニューロブラスト静止退出を媒介する.
- インスリン/IGF受容体の経路は,栄養と幹細胞再活性化との間の重要なリンクです.
- ニューロブラストの増殖は,この経路を操作することによって,システミックコントロールから切り離すことができます.
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