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血管生成のグリコムとトランスクリプトームの調節

Rania Harfouche¹, Dirk M Hentschel¹, Stephanie Piecewicz¹

¹Department of Medicine (R.H., D.M.H., S.P., S.B., S.S.), Brigham and Women's Hospital, Boston, Mass; Department of Molecular Medicine and Pathology (C.P.), University of Auckland, Auckland, New Zealand; Department of Biological Engineering (D.E., T.K., R.S.), Massachusetts Institute of Technology, Cambridge, Mass; and Harvard-MIT Division of Health Sciences and Technology (R.H., S.P., S.B., D.E., T.K., R.S., S.S.), Cambridge, Mass.

|October 28, 2009

まとめ

この研究では,ヘパラン硫酸グリコサミノグリカンと遺伝子発現がどのように相互作用して血管形成 (血管新生) を調節するかを明らかにしています. これらの相互作用を調節することで,不血症状態における治療的血管化の可能性が生まれます.

科学分野:

バイオケミストリーバイオケミストリー
発達生物学発達生物学について
分子生物学は分子生物学である.

背景:

治療的血管新生は,缺血性疾患の治療のための有望な戦略です.
細胞表面のグリコーム,特にヘパラン硫酸グリコサミノグリカン (HSG),およびトランスクリプトームは,血管新生を調節する役割について調査されています.

研究の目的:

HSGとトランスクリプトームによる血管生成の共同調節を解明する.
血管形成中のグリコムとトランスクリプトームの相互作用を探求する.

主な方法:

胚性幹細胞が内皮細胞に微分化する.
小型のヘアピンRNAを用いてN-デアセチラゼ/N-スルフォトランスフェラーゼ1 (NDST1) のノックダウン.
ゼブラフィッシュの胚を用いたインビボ研究.
遺伝子発現パターンを特定するためのマイクロアレイ分析.

主要な成果:

NDST1レベルと相関するHSG硫化は,内皮細胞の分化に不可欠です.
NDST1のノックダウンまたはHSGの改変により,胚性幹細胞の分化とゼブラフィッシュの血管化が損なわれた.
遺伝子発現分析は,グリコカリックス調節と細胞シグナル伝達,生存,そして運命決定を結びつける経路を明らかにし,フォークヘッドボックスO3A/5とインスリン型の成長因子を含む.

結論:

この研究は,血管新生過程でグリコームとトランスクリプトームの間の新しい相互作用を示しています.
細胞のグリコ-マイクロ環境をターゲットにすることは,治療的血管化戦略の潜在的な道を示しています.

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