莱索酶M阳性单细胞通过血管新生素II诱导的动脉高血压和血管功能障碍进行介导
Philip Wenzel1, Maike Knorr, Sabine Kossmann
12(nd) Medical Clinic, University Medical Center Mainz, Germany. wenzelp@uni-mainz.de
Circulation
|August 31, 2011
概括
透的单细胞和巨细胞,而不是中性粒细胞,是 ангиотензин II 诱导的高血压和血管功能障碍的关键驱动因素. 耗尽这些细胞会降低血压和氧化应激,突出显示它们的治疗潜力.
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
- 高血压研究 高血压研究
背景情况:
- ангиотензин II (ATII) 是一种与高血压和血管炎症相关的血管收缩剂.
- 不同骨髓单细胞细胞和NADPH氧化酶源在ATII诱导的高血压中的特定作用仍然不清楚.
研究的目的:
- 确定骨髓单细胞在 ангиотензин II 诱导的动脉高血压中的作用.
- 确定 ангиотензинII介导的血管功能障碍中反应性氧物种的主要来源.
主要方法:
- 使用诱导性白喉毒素受体小鼠 (LysM(iDTR)) 来选择性地耗尽酶M阳性 (LysM(+)) 髓单细胞.
- 服用安二醇来诱导高血压,并评估血压,血管功能和氧化应激.
- 利用流动细胞计,放射测量,大动脉环研究,化学发光和西部涂抹来分析细胞透,血压,血管反应和NADPH氧化酶表达.
主要成果:
- ангиотензин II 增加了小鼠大动脉中的循环单细胞和中性粒细胞.
- 选择性消耗LysM(+) 细胞减少了单细胞透,减轻了 ангиотензинII诱导的高血压和血管功能障碍.
- LysM(+) 细胞的枯竭也减少了血管超氧化物形成和NADPH氧化酶子单元的表达.
结论:
- 透的单细胞和巨细胞,具有亲炎性表型的特征,对于 ангиотензин II 诱导的血管功能障碍和动脉高血压至关重要.
- 中性粒细胞在这个过程中没有发挥重要作用.
- 针对这些特定的单细胞/巨细胞群体可能为高血压提供治疗策略.
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