骨髄由来細胞は血管炎症に寄与しますが,滑らかな筋肉の細胞系統に微分化することはありません
Hiroshi Iwata1, Ichiro Manabe, Katsuhito Fujiu
1Department of Cardiovascular Medicine, Graduate School of Medicine, University of Tokyo, Tokyo, Japan.
Circulation
|November 3, 2010
まとめ
損傷した動脈における滑らかな筋肉α-アクチンを発現する骨髄由来細胞は,滑らかな筋肉細胞ではなく炎症性モノサイトです. これらの細胞は血管の再編成に寄与しますが,明確な滑らかな筋肉の系統を採用しません.
科学分野:
- 血管生物学 血管生物学
- 細胞系統 細胞系統 細胞系統
- 免疫学 免疫学とは
背景:
- 骨髄由来細胞は,ネオインティマに浸透し,滑らかな筋肉 (SM) 細胞に微分化すると仮定されています.
- 以前の研究では,これらの骨髄由来の精密な系統を特定する技術的な制限に直面しました.
研究 の 目的:
- 血管損傷における滑らかな筋肉 (SM) α-アクチンを発現する骨髄由来細胞の系統を明らかにする.
- これらの細胞が明確な滑らかな筋肉細胞に微分化するかどうかを判断する.
主な方法:
- SMミオシン重鎖 (SM-MHC) に対する特定の抗体と,SM-MHCとSMα-actinに対するレポーター遺伝子マウスラインを使用した.
- ワイヤの損傷によるネオインティマ,アポリポプロテインE (((-/-) のマウスにおける血管損傷,心臓移植の血管病変モデルを分析した.
- 表面マーカー (CD115,CD11b,F4/80,Ly-6C) を使用した骨髄由来細胞のフェノタイプと,炎症に関連する遺伝子発現の評価.
主要な成果:
- ネオインティマでSMα-アクチンを発現する骨髄由来細胞は,傷害後の長期にわたり,決定的なSM-MHCマーカーを発現しなかった.
- これらのSMα-アクチンを発現する細胞は,炎症性モノサイト (CD115(+) CD11b(+) F4/80(+) Ly-6C(+)) のフェノタイプを示した.
- 採用された炎症性モノサイトは,損傷した動脈でSMα-アクチンを発現し,炎症遺伝子の発現は,これらの細胞を持つ領域で上昇しました.
結論:
- 骨髄由来SMα-アクチン (((+) 細胞は主にモノサイト/マクロファージ系である.
- これらの細胞は,血管の再編成に役割を果たします.
- これらの細胞が決定的な滑らかな筋肉の細胞系統を取得することは非常に不可能です.
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