アポリポプロテインJ/クラスタリンは,血管損傷後の血管の滑らかな筋肉細胞に誘導されます
1First Department of Internal Medicine, Faculty of Medicine, Kagoshima University, Kagoshima, Japan.
Circulation
|September 19, 2001
まとめ
アポリポプロテインJ (apoJ) は,血管損傷後に著しく上位調節され,滑らかな筋肉細胞の増殖と移動を促進します. これは,アニオプラスティック手術後のレステノシスにApoJが重要な役割を果たしていることを示唆しています.
科学分野:
- 分子生物学は分子生物学である.
- 心血管研究 循環器科の研究
- 遺伝子発現分析 遺伝子発現分析
背景:
- パーキュタヌス・トランスルミナル冠動脈血管形成術 (PTCA) の後の血管静止症は,効果的な治療のために分子メカニズムを理解することが必要である.
- 血管静止症に関与する遺伝子を特定することは,新しい治療戦略の開発に不可欠です.
研究 の 目的:
- 血管回復症の発達に関与する遺伝子を特定する.
- アポリポプロテインJ (apoJ) /クラスタリンの血管損傷反応における役割を調査する.
主な方法:
- バルーンで傷ついたウサギの大動脈モデルで,差異的ハイブリダイゼーションが採用されました.
- 遺伝子とタンパク質の発現を分析するために,ノース・ブロット,ウエスタン・ブロット,免疫ヒスト化学,およびイン・シット・ハイブリダイゼーションが使用されました.
- ウサギの滑らかな筋肉細胞 (SMC) の安定した転移が,アポジョイ機能の研究のために行われました.
主要な成果:
- 6つのcDNAクローンは,傷害後のアップレギュレーションを受け,5つの遺伝子が構成的に発現し,アップレギュレーションを受けた.
- アポリポプロテインJ (apoJ) のmRNAおよびタンパク質発現は,気球損傷後に有意に誘発され,それぞれ24時間および2〜8週間でピークに達しました.
- ApoJの発現は,メディアとネオインティマの滑らかな筋肉細胞に局限され,その発現はSMCの増殖と移住を刺激しました.
結論:
- アポリポプロテインJ (apoJ) は,血管損傷後のメディアとネオインティマで劇的に誘発されます.
- この発見は,アポJが血管新生手術後のレステノシスの病原化に有意に寄与することを示唆しています.
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