低氧/低氧化刺激了人类大动脉内皮细胞中的细胞内振荡
1Department of Medicine, Division of Cardiology, Johns Hopkins Bayview Medical Center, Johns Hopkins University School of Medicine, Baltimore, MD 21224-2780, USA.
Circulation
|November 15, 2000
概括
后毒性复氧化触发了内皮细胞中的振荡. 这些由过氧化启动的振荡在缺血/反事件期间对信号传导至关重要.
科学领域:
- 心血管生物学 心血管生物学
- 细胞生理学 细胞生理学
- 生物化学 生物化学
背景情况:
- 以前的研究表明过氧化在刺激内皮振荡中的作用.
- 这项研究调查了后毒性复氧化是否也会在血管内皮细胞中诱导这些振荡.
研究的目的:
- 为了确定缺氧后的再氧化是否会刺激人类大动脉内皮细胞中的细胞内 ([Ca(2+) ](i)) 振荡.
- 阐明重新氧化诱导的振荡所涉及的机制和信号通路.
主要方法:
- 人类大动脉内皮细胞经历了缺氧,随后再氧化.
- 细胞内水平和振荡被用Indo1光测量.
- 用特定的抑制剂向像NAD(P) H氧化酶和信号通路这样的酶来剖析底层机制.
主要成果:
- 低氧增加了基底细胞内水平.
- 重氧化在大多数细胞中诱导了重复的细胞内振荡,持续超过60分钟.
- 这些振荡取决于细胞内释放和细胞外,并被NAD(P) H氧化酶抑制剂和催化酶特别抑制,这表明过氧化的作用.
结论:
- 后毒性复氧化刺激了内皮细胞中强大的细胞内振荡.
- 这些振荡取决于细胞内储存和细胞外流入.
- NAD(P) H氧化酶衍生的过氧化可能会启动这些振荡,可能在缺血/反信号传导中发挥重要作用.
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