ATP結合カセットトランスポーターA1の発現とアポリポプロテインA-Iの結合は,インティマ型動脈平滑筋細胞に障害がある
Hong Y Choi1, Maziar Rahmani, Brian W Wong
1Department of Medicine, Heart and Lung Institute, St. Paul's Hospital, 1081 Burrard Street, Vancouver, BC, Canada.
Circulation
|June 17, 2009
まとめ
内側の滑らかな筋肉細胞 (SMC) のATP結合カセットトランスポーターA1 (ABCA1) 発現の低下は,コレステロールの流出を阻害し,動脈硬化における泡細胞形成に貢献します. これは,ABCA1機能不全が親密なSMCの鍵であることを示唆しています.
科学分野:
- 心血管生物学 心血管生物学
- 動脈硬化症の研究研究
- 細胞脂質代謝について
背景:
- 動脈硬化性病変における滑らかな筋肉細胞 (SMC) はコレステロールを蓄積し,泡細胞を形成する.
- ATP結合カセットトランスポーターA1 (ABCA1) は,細胞のコレステロール流出に重要な役割を果たしています.
研究 の 目的:
- モデルとヒトの動脈硬化動脈から,親密なおよび中間的なSMCにおけるABCA1発現と活動を調査する.
- 滑らかな筋肉の泡細胞形成におけるABCA1の役割を理解するために.
主な方法:
- 比較されたABCA1発現と脂質流出は,モデルインティマル対メディアルSMCで.
- 人間の動脈硬化冠動脈内側と中部層のABCA1レベルを分析した.
- 内部SMCにおける脂質処理に対するABCA1アップレギュレーションの影響を評価した.
主要な成果:
- モデルの親密なSMCは,中間SMCと比較して,ABCA1発現の低下,脂質流出の障害,およびアポリポプロテインA-I結合の低下を示した.
- 人間の動脈硬化性親密な層は,中間層と比較して,ABCA1 mRNAとタンパク質のレベルが低下しました.
- ABCA1発現の強化は,親密なSMCにおける脂質流出や高密度脂質タンパク質形成を回復させず,本質的な結合因子の欠如を示唆した.
結論:
- ABCA1の発現は,モデルおよびヒトの親密なSMCの両方で著しく減少しています.
- 腸内SMCにおけるABCA1の活性低下は,コレステロールの蓄積と泡状細胞の形成に寄与する.
- インティマルSMCには,ABCA1媒介のコレステロール流出に必要な重要な要因が欠けている可能性があります.
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