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单细胞化学吸引蛋白-1在由长期阻断氧化合成引起的心血管重塑中的作用.

M Koyanagi1, K Egashira, S Kitamoto

  • 1Department of Cardiovascular Medicine, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.

Circulation
|November 1, 2000
PubMed
概括

单细胞化学吸引蛋白-1 (MCP-1) 驱动血管炎症和介质缩在与N:(omega) -nitro-L-arginine甲基 (L-NAME) 治疗的老鼠. 然而,MCP-1不参与纤维化发育.

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科学领域:

  • 心血管生物学 心血管生物学
  • 炎症研究 炎症研究
  • 血管生物学 血管生物学

背景情况:

  • 通过L-NAME对内皮氧化 (NO) 合成的慢性抑制会在老鼠中诱导血管炎症和动脉硬化.
  • 关键的炎症变化包括单细胞透和单细胞化学吸引蛋白-1 (MCP-1) 表达.
  • 对于MCP-1在L-NAME诱导的心血管改造中的特定作用尚不清楚.

研究的目的:

  • 阐明MCP-1在L-NAME诱导的心血管重塑中的作用.
  • 为了确定MCP-1是否调解单细胞招募和随后的血管变化.
  • 调查MCP-1在介质厚和纤维化发展中的参与.

主要方法:

  • 在接受L-NAME治疗的老鼠中使用了特定的单克隆抗MCP-1中和抗体.
  • 在血管内皮细胞和单细胞中的量化MCP-1mRNA表达.
  • 评估了抗MCP-1抗体治疗对炎症,介质厚,周血管纤维化,TGF-β) mRNA表达和静脉压的影响.

主要成果:

  • 在炎症病变内的血管内皮细胞和单细胞中观察到MCP-1 mRNA表达的增加.
  • 用抗MCP-1抗体治疗可以预防L-NAME诱导的早期炎症.
  • 抗MCP-1抗体治疗减少了冠状动脉血管中介厚度,但没有影响周围血管纤维化或TGF-β) mRNA表达.

结论:

  • 在这个模型中,MCP-1对于单细胞招募和介质增厚的发展至关重要.
  • 纤维化发展似乎由MCP-1以外的其他因素调节,可能包括TGF-β.
  • 这些发现突出了MCP-1作为L-NAME诱导心血管病理的特定方面的关键调解者.