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RIPK1は,アポプトーシスとネクロプトーシスを阻害することによって,上皮の恒常性を維持する
Marius Dannappel1, Katerina Vlantis1, Snehlata Kumari1
11] Institute for Genetics, Centre for Molecular Medicine (CMMC), and Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, 50931 Cologne, Germany [2].
Nature
|August 19, 2014
まとめ
受容体相互作用タンパク質キナーゼ1 (RIPK1) は,細胞のプログラム死亡と上皮組織の炎症を防ぐ. RIPK1はRIPK1に該当する.
科学分野:
- 細胞生物学 細胞生物学
- 免疫学 免疫学とは
- 発達生物学 発達生物学とは
背景:
- ネクロプトーシスは,発達,ホメオスタシス,免疫,炎症に関与する重要なプログラム細胞死経路です.
- RIPK1は炎症および細胞死シグナル伝達に関与することが知られており,そのキナーゼ活性がRIPK3媒介性死滅を引き起こす.
研究 の 目的:
- ホメオスタシスを調節し,障壁組織における炎症を予防する際に,RIPK1のキナーゼ独立性脚本機能の役割を調査する.
- 皮質細胞のアポトーシスと死滅を抑制するRIPK1のメカニズムを解明する.
主な方法:
- 生成された腸上皮細胞 (IEC) 固有のRIPK1ノックアウトマウス.
- FADDアブレーションとRIPK1キナーゼイナクティブノックインモデルを使用した.
- エピダーミス特異的な RIPK1 ノックアウト実験を行いました.
- 微生物群とMyD88シグナル伝達との関係で病理学を分析した.
- TNFR1欠乏症の影響を評価しました.
主要な成果:
- IEC特有のRIPK1ノックアウトは,微生物群とMyD88シグナル伝達とは無関係にアポトーシス,小胞縮,細胞喪失,早死を引き起こした.
- エピテリアのFADDの除去により,RIPK1のノックアウトマウスの早期死亡が救われたが,RIPK1とFADDの欠乏が併合され,RIPK3依存性死滅と炎症を引き起こした.
- RIPK1キナーゼの不活性が,FADD欠乏性の上皮細胞炎症を部分的に救出しただけで,RIPK3依存性ネクロプトーシスは部分的にRIPK1キナーゼの活性を必要とすることを示しています.
- Epidermis-specific RIPK1ノックアウトは,ケラチノサイトアポトーシスとネクロプトーシスを引き起こし,RIPK3欠乏によって予防された重度の皮膚炎を引き起こしました.
結論:
- RIPK1のキナーゼに依存しない脚立機能は,上皮質の恒常性を維持し,障壁組織の炎症を予防するために不可欠です.
- RIPK1は,RIPK3媒介によるケラチノシートの死滅を vivo で抑制する.
- ネクロプトーシスは,アポプトーシスよりも強力な炎症の引き金です.
- RIPK1は,上皮細胞生存,ホメオスタシス,腸および皮膚の炎症の主調節体として作用します.
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