C反応性タンパク質は,アポリポプロテインE欠乏マウスの動脈硬化症の進行を加速する
Antoni Paul1, Kerry W S Ko, Lan Li
1Division of Diabetes, Endocrinology & Metabolism, Department of Medicine, Baylor College of Medicine, Houston, Tex 77030, USA.
Circulation
|January 28, 2004
まとめ
人間のC反応性タンパク質 (CRP) は,マウスの動脈硬化を加速する. この研究は,CRPが大動脈の病変の発生を促進し,そのサイズと炎症の細胞マーカーを増加させるという in vivo の証拠を提供します.
科学分野:
- 心血管研究 循環器科の研究
- 免疫学 免疫学とは
- 遺伝学 遺伝学とは
背景:
- 血のC反応性タンパク質 (CRP) は,動脈硬化症の既知の予測因子である.
- 以前の研究では,CRPのプロアテロゲン作用を確認するインビボの証拠が不足していました.
研究 の 目的:
- アポリポタンパク質E欠乏マウスにおける動脈硬化症の発達に対するヒトCRPトランスゲン発現のインビボ効果を調査する.
主な方法:
- 人間のCRPトランスゲン (tg) を持つアポリポプロテインE欠乏症 (apoE-/-) のマウスを利用した.
- 基礎およびテルペンチン刺激条件での動脈硬化症の評価.
- 分析された大動脈動脈硬化病変のサイズ,C3の堆積,血管細胞粘着分子-1,コラーゲン,およびアンジオテンシン1型受容体 (AT1-R) の発現.
主要な成果:
- 人間のCRPトランスゲン発現は,アポE-/-マウスにおける大動脈動脈硬化病変のサイズを大幅に増加させた.
- 病変内ではCRPと補足C3の堆積が上昇した.
- AT1-R,血管細胞粘着分子-1,およびコラーゲンの発現の増加は,CRP発現するマウスの病変で観察されました.
- 血圧の有意な差は認められず,局所的な効果を示した.
結論:
- 人間のCRPトランスゲンの発現は,アポE-/-マウスにおける大動脈動脈硬化を加速する.
- CRPは体内ではプロアテロゲン性であり,補完体の活性化と,動脈硬化病変内の炎症マーカーとAT1-Rの発現の増加と関連しています.
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