尼菲迪平通过血管光滑肌肉细胞依赖的途径间接上调内皮细胞中超氧化物脱酶的表达
Keisuke Fukuo1, Jin Yang, Osamu Yasuda
1Department of Geriatric Medicine, Osaka University Medical School, Suita, Osaka, Japan. fukuo@geriat.med.osaka-u.ac.jp
Circulation
|July 18, 2002
概括
像尼菲迪平这样的抗体通过增加内皮细胞 (ECs) 中的超氧化失调酶 (SOD) 来改善内皮功能. 这种效应是由血管光滑肌细胞 (VSMCs) 介导的,它们释放血管内皮生长因子 (VEGF).
科学领域:
- 心血管研究研究心血管研究
- 内皮细胞生物学 内皮细胞生物学
- 顺滑肌细胞功能 顺滑肌细胞功能
背景情况:
- 已知抗体可以改善心血管疾病中的内皮功能障碍.
- 内皮细胞中抗体的特定受体仍未确定.
- 血管光滑肌细胞 (VSMCs) 假设调解抗体对内皮细胞 (ECs) 的作用.
研究的目的:
- 调查VSMC是否调节内皮超氧化物失调酶 (SOD) 活动和表达的对手尼菲迪平的调节.
- 阐明血管内皮生长因子 (VEGF) 在这个过程中的作用.
主要方法:
- 关于EC和VSMC的共同文化研究.
- 用尼菲迪平 (nifedipine) 治疗,尼菲迪平是一种抗体.
- 测量SOD活动和表达.
- 对血管内皮生长因子 (VEGF) 生产的评估.
- 布拉迪基宁B2受体对抗剂 (HOE-140) 和VEGF中和抗体的使用.
主要成果:
- 当与VSMC共同培养时,nifedipine在EC中调节了SOD表达和活性,但当单独培养时不会.
- 尼菲迪平刺激了VSMCs的VEGF产量,而HOE-140则阻止了这种产量.
- 在EC中,VEGF中和抗体抑制了尼菲迪平诱导的SOD上调.
- 再组合VEGF在EC中增加了SOD表达.
- VSMC超增强了EC中的氧化 (NO) 生产,这种影响取决于SOD.
结论:
- 抗体尼菲迪平间接上调内皮SOD的表达.
- 这种上调是通过邻近的VSMCs的VEGF刺激来调节的.
- 这些发现提供了关于抗体在心血管疾病中的有益机制的见解.
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