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'https://openalex.org/W1973442679'], 'abstract_inverted_index': {'脳が損傷を受けたり神経変性疾患に陥った場合,ミクログリアは活性化し病変部位に集積する.活性化ミクログリアの主な役割は,死細胞の除去や免疫担当細胞として脳組織を修復することである.しかしながら,活性化ミクログリアから産生される過剰量のNOは,神経変性過程でみられる神経障害の重要なメディエーターと考えられている.NOによる細胞死のメカニズムについては十分には解明されておらず,標的が何であるかも分かっていない.一般にNO毒性は,ミトコンドリアの機能不全やDNA障害/p53経路を介して起こると考えられている.著者らは,p53ノックアウトマウス由来のミクログリア細胞株MG5を用いてNO毒性のメカニズムについて解析した.MG5をLPS/IFNγで処理すると,iNOSが誘導され,アポトーシスが起こった.この時,小胞体(ER)ストレス誘導性のアポトーシスに関与するCHOP/GADD153が誘導されることを見いだした.また,ERストレスによって誘導されることが知られるBiP/Grp78も誘導された.これらの結果より,MG5ミクログリアにおけるNO依存性アポトーシスは,CHOPの誘導を含む小胞体ストレス経路を介して起こっており,p53とは無関係であることが明らかとなった.このように,過剰な活性化によって引き起こされたミクログリア自身のアポトーシスは,近傍に位置する脆弱な神経細胞を殺さないようにする,ミクログリアの重要な自己制御機構かもしれない.一方,最近の報告によると,ミクログリアは中枢神経系において2種以上のヘテロな細胞集団から成ることが示唆されている.著者らは,type-1とtype-2ミクログリアを分離し,それぞれの海馬神経細胞に対する影響を解析した.活性化type-1ミクログリアは,iNOSを著しく誘導して神経細胞死を引き起こしたが,同様に活性化したtype-2ミクログリアでは,そのような神経傷害作用は観察されなかった.中枢神経系の炎症過程においては,性質の異なるミクログリアサブタイプが異なった作用を示す可能性がある.': [0]}, 'cited_by_api_url': 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