激活的单细胞诱导平滑肌肉细胞死亡:巨细胞殖民地刺激因子和细胞接触的作用
Puvi N Seshiah1, Dean J Kereiakes, Sanjay S Vasudevan
1Division of Cardiology, Department of Medicine, Emory University, Atlanta, GA, USA.
Circulation
|January 16, 2002
概括
单细胞和巨细胞殖民地刺激因子 (M-CSF) 触发血管光滑肌肉细胞 (VSMC) 死亡. 药物abciximab针对Mac-1受体,可以阻止这一过程,为心血管事件提供潜在的治疗途径.
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
- 细胞病理学细胞病理学
背景情况:
- 斑块破坏是冠状动脉栓塞和急性冠状动脉综合征的关键事件.
- 血管光滑肌细胞 (VSMC) 的损失导致斑块不稳定.
- 由巨细胞殖民地刺激因子 (M-CSF) 激活的单细胞/巨细胞 (MMs) 与VSMC死亡有关.
研究的目的:
- 调查M-CSF激活MMs在VSMC亡中的作用.
- 确定预防M-CSF诱导的VSMC死亡的潜在治疗点.
主要方法:
- 在MMs和/或M-CSF的存在下量化了VSMC亡.
- 评估了abciximab,tirofiban,eptifibatide和抗CD-18抗体对VSMC亡的作用.
- 评估了MM-VSMC相互作用和M-CSF度依赖.
主要成果:
- 与对照组相比,M-CSF激活的MMs显著增加了VSMC亡.
- 在M-CSF刺激的VSMC杀死中,MM细胞接触是必不可少的.
- 绑定Mac-1到MMs的Abciximab显著降低了VSMC的亡.
- 不抑制Mac-1的蒂罗非班和埃普蒂菲巴提德不能阻止VSMC的亡.
结论:
- 单细胞和M-CSF诱导VSMC的亡.
- 抑制Mac-1受体的药物,如abciximab,可以对抗这种亡过程.
- 准Mac-1通路可能为急性冠状动脉综合征提供治疗策略.
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