支架诱导的白细胞整合素Mac-1的表达和激活与新极端的厚化和复缩有关
Teruo Inoue1, Toshihiko Uchida, Isao Yaguchi
1Department of Cardiology, Koshigaya Hospital, Dokkyo University School of Medicine, 2-1-50 Minamikoshigaya, Koshigaya City, Saitama 343-8555, Japan. inouet@dokkyomed.ac.jp
Circulation
|April 1, 2003
概括
冠状动脉支架激活了Mac-1 (CD11b/CD18),这是一种白细胞整合素,涉及到新极端增生症. 这种激活预测了晚期的光线损失和复原,这表明炎症起着关键作用.
科学领域:
- 心血管生物学 心血管生物学
- 免疫学 免疫学 免疫学
- 集成的信号传输.
背景情况:
- 增加β2整合蛋白Mac-1 (CD11b/CD18) 表达与冠状动脉干预后的新极端增生有关.
- 麦克-1在静止病病理生理学中的确切作用尚不清楚.
- 冠状动脉支架可能会诱导Mac-1激活,这对于高亲和度受体-连接体相互作用至关重要.
研究的目的:
- 为了调查冠状动脉支架是否会触发Mac-1激活.
- 为了确定Mac-1激活和支架后晚期光损失之间的关联.
- 探索Mac-1在炎症反应中的作用,有助于复原.
主要方法:
- 使用流细胞计分析了白细胞上的CD11b表达和8B2结合 (Mac-1激活标志物).
- 从62名冠状动脉支架后患者的冠状动脉鼻和大腿静脉中采集了血液样本.
- 定量冠状动脉血管学评估了晚期光线损失.
主要成果:
- 经心脏CD11b表达和8B2结合在支架后显著增加,在48小时达到峰值.
- 这些增加在患有复原症的患者中更为明显.
- 麦克-1激活 (8B2结合) 是晚期光损失 (R=0.55,P<0.001) 最强的独立预测因素.
结论:
- 冠状动脉支架导致Mac-1上调和早期激活.
- 麦克-1激活与晚期光线损失和复原有显著的关联.
- 这些发现支持准白细胞的招募,以防止新极端的厚化和复原.
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