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プロスタグランジン合成酵素2遺伝子の障害は,マウスで重度の腎臓病理を引き起こす
S G Morham1, R Langenbach, C D Loftin
1Department of Pathology, University of North Carolina at Chapel Hill 27599-7525, USA.
Cell
|November 3, 1995
まとめ
サイクロオキシゲナーゼ2 (COX-2) が欠けているマウスは,正常な炎症反応を示しますが,腎臓疾患と炎を発症します. これは,COX-2が炎症以外の役割を持っていることを示唆しています.
科学分野:
- バイオケミストリー バイオケミストリー
- 免疫学 免疫学とは
- 遺伝学 遺伝学とは
背景:
- サイクロオキシゲナーゼ2 (COX-2) は炎症的刺激によって誘発され,炎症の重要な媒介者と考えられています.
- その同型であるサイクロオキシゲナーゼ1 (COX-1) は,構成的に発現し",家政"の機能を果たしている.
- COX-1とCOX-2は,非ステロイド性抗炎症薬 (NSAID) の治療標的である.
研究 の 目的:
- COX-1およびCOX-2イソフォームの異なる生理学的役割を調査する.
- COX-2の不在を研究することによって,COX-2の機能をin vivoで理解する.
主な方法:
- ホモログな再結合は,COX-2 (Ptgs2) をコードするマウス遺伝子を遺伝的に破壊するために使用されました.
- COX-2 が欠けていたマウスは,炎症刺激に対する反応と全体的な健康状態を分析した.
主要な成果:
- COX-2 欠乏したマウスは,テトラデカノイルホルボルアセテートとアラキドン酸に正常な炎症反応を示した.
- しかし,COX-2ノックアウトマウスは重度の腎不全 (腎疾患) を発症した.
- また,これらのマウスは炎に敏感であることが判明しました.
結論:
- COX-2は腎臓の健康を維持し,炎の予防に重要な役割を果たします.
- COX-2の生理学的機能は,炎症を媒介する確立された役割を超えて広がっています.
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