瘤坏死因子-α通过cAMP途径促进血管细胞的体外化
1Division of Cardiology, Departments of Medicine and Physiology, UCLA School of Medicine, Los Angeles, CA 90095-1679, USA. ytintut@ucla.edu
Circulation
|November 22, 2000
概括
瘤坏死因子-α (TNF-α) 通过诱导血管细胞中的骨质细胞分化来促进血管化. 这一过程涉及cAMP通路并增强矩阵矿化,这表明TNF-alpha在动脉样硬化中的作用.
科学领域:
- 心血管生物学 心血管生物学
- 细胞生物学 细胞生物学
- 生物化学 生物化学
背景情况:
- 血管化是动脉样硬化的一个标志.
- 瘤坏死因子-α (TNF-α),在动脉样硬化病变中的细胞因子,调节骨的形成.
- 在血管化中TNF-alpha的作用需要研究.
研究的目的:
- 研究TNF-alpha在体外血管化中的作用.
- 确定TNF-α是否促进血管细胞的骨质细胞分化.
主要方法:
- 牛大动脉光滑肌细胞被用TNF-alpha治疗.
- 使用性酸酶活性和合物纳入来评估骨质细胞分化和矿化.
- 分析了蛋白质激酶A抑制剂 (KT5720) 和cAMP水平.
- 电泳运动转移试验确定了转录因子结合.
主要成果:
- TNF-α诱导了类似骨质细胞的形态,并增强了性酸酶活性和mRNA表达.
- 持续的TNF-α治疗增加了矩阵矿化.
- 抑制蛋白激酶A减弱的TNF-α诱导作用.
- TNF-α提高了细胞内cAMP水平,并增强了Osf2,AP1和CREB的DNA结合.
结论:
- 在体外,TNF-α促进了血管化.
- 这种效应是通过促进血管细胞中的骨质母细胞分化来实现的.
- 该cAMP途径参与TNF-α诱导的血管化.
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