皮表皮生长因子通过脂酶A2/5-氧基酶介导的Leukotriene C4生产激活通道
M P Peppelenbosch1, L G Tertoolen, J den Hertog
1Hubrecht Laboratory, Netherlands Institute for Developmental Biology, Utrecht.
Cell
|April 17, 1992
概括
皮表皮生长因子 (EGF) 通过一种新的途径触发 (Ca2+) 流入,涉及白血C4生产. 这种依赖氧酶的机制对于EGF诱导的细胞反应至关重要.
科学领域:
- 细胞生物学 细胞生物学
- 分子生物学分子生物学
- 生物化学 生物化学
背景情况:
- 众所周知,表皮生长因子 (EGF) 在各种细胞类型中诱导 (Ca2+) 流入.
- 导致EGF诱导的Ca2+流入的精确分子机制在很大程度上仍未解决.
- 了解这些通路对于破译生长因子信号至关重要.
研究的目的:
- 为了阐明介于EGF诱导的Ca2+流入的信号通路.
- 调查氧基酶和白血C4在EGF作用中的作用.
- 确定这种途径在生长因子诱导的细胞事件中的特异性.
主要方法:
- 抑制脂氧酶活性,以评估其在EGF信号传递中的作用.
- 模仿氧酶活性,观察对Ca2+通道的影响.
- 在EGF刺激后测量细胞内白血素C4的积累.
- 评估EGF诱导的膜超极化,JunB原基因表达和细胞质化.
主要成果:
- 脂氧酶抑制消除了EGF诱导的Ca2+通道活性,而其诱导则模仿了该效应.
- 添加 C4 叶可烯完全复制了 EGF 激活 Ca2+ 通道的能力.
- 刺激EGF导致细胞内白血素C4水平的快速增加.
- EGF诱导的Ca2+依赖性膜超极化和JunB表达依赖于脂氧基酶,但细胞质化不是.
结论:
- 通过PLA2/5-lipoxygenase介导的Leukotriene C4生产代表了增长因子作用中的新和特定的信号转导途径.
- 这一途径对于调解细胞对EGF的关键反应至关重要,包括Ca2+流入和膜电位变化.
- 这些发现突出了一个新的机制,将生长因子刺激与细胞内动态和基因表达联系起来.
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