酶降解,非氧化LDL诱导人体血管光滑肌肉细胞激活,泡细胞转化和增殖
M Klouche1, S Rose-John, W Schmiedt
1Institute of Medical Microbiology, University of Mainz, Germany. klouche@mail.uni-mainz.de
Circulation
|April 19, 2000
概括
酶改性LDL (E-LDL) 触发了血管光滑肌肉细胞 (SMC) 的增殖,并改变了它们的基因表达,导致早期动脉样硬化病变的发展.
科学领域:
- 心血管生物学 心血管生物学
- 动脉样硬化研究 动脉样硬化研究
- 细胞和分子医学是细胞和分子医学.
背景情况:
- 对LDL的酶性,非氧化性修改会产生一种异构的形式 (E-LDL).
- E-LDL激活补体和巨细胞,在早期动脉样硬化病变中出现.
研究的目的:
- 研究E-LDL对人类血管光滑肌细胞 (SMC) 的动脉性影响.
主要方法:
- 在SMC中评估E-LDL积累.
- 测量了化学因子和炎症蛋白的基因表达.
- 分析了gp130和IL-6受体 (IL-6R) 家族的信号传导.
- 研究了E-LDL诱导的SMC扩散机制.
主要成果:
- 在SMC中积累的E-LDL,选择性诱导单细胞化疗蛋白-1.
- E-LDL刺激了gp130的表达和IL-6的分泌.
- 通过自克林生长因子电路和IL-6/sIL-6R转信号,E-LDL促进了SMC的扩散.
- 巨细胞衍生的IL-6和可溶性IL-6受体 (sIL-6R) 增强了SMC的扩散.
结论:
- E-LDL诱导SMC变化的特征是不断演变的动脉样硬化病变.
- E-LDL有助于在早期动脉样硬化中观察到的细胞变化.
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