ネトリン受容体UNC5Bは,血管系の形態変異を制御する誘導イベントを媒介する

Xiaowei Lu¹, Ferdinand Le Noble, Li Yuan

¹Department of Biological Sciences, Howard Hughes Medical Institute, Stanford University, Stanford, California 94305, USA.

Nature

|October 29, 2004

まとめ

排斥性ネトリン受容体UNC5Bは,血管の発達を誘導する. その障害は,異常な血管の分岐とナビゲーションを引き起こし,UNC5Bを明らかにします.

科学分野:

発達生物学発達生物学について
血管生物学血管生物学
神経科学は神経科学である.

背景:

血管と神経は,似たような複雑で枝分かれした解剖学的構造を示しています.
精密な誘導機構は,血管系と神経系の両方の適切な配線に不可欠です.
いくつかのアクソン誘導レギュレータは内皮細胞に存在しますが,血管誘導におけるそれらの保存された役割は不明です.

研究の目的:

血管発達におけるネットリン受容体UNC5Bの役割を調査する.
UNC5Bが内皮細胞の誘導信号として機能するかどうかを判断する.

主な方法:

マウスでの遺伝子破壊研究 (Unc5bノックアウト).
ゼブラフィッシュの遺伝子破壊研究 (Unc5bとネットリン-1aのノックアウト).
内皮の先端細胞のフィロポディアの拡張,血管の分岐,およびナビゲーションの分析.

主要な成果:

UNC5Bは,内皮の先端細胞によって発現します.
Unc5b (マウス) またはUnc5b/netrin-1a (ゼブラフィッシュ) の破壊は,異なったフィロポディアの拡張,過剰な船の分岐,および異常な航海をもたらしました.
ネトリン-1が誘発した内皮フィロポディアス収縮は,特にUNC5Bの存在下で発生した.

結論:

UNC5Bは,内皮細胞における排斥性ネットリン受容体として作用する.
UNC5Bは,血管形態変異と誘導を制御する上で重要な役割を果たします.
この研究は,神経系と血管系との間の保存されたガイドメカニズムを強調しています.

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