皮肤上生长因子诱导的actin重塑是由5-lipoxygenase和cyclooxygenase产物调节的
M P Peppelenbosch1, L G Tertoolen, W J Hage
1Hubrecht Laboratory, Netherlands Institute for Developmental Biology, Utrecht.
Cell
|August 13, 1993
概括
皮表皮生长因子 (EGF) 通过阿拉基酸代谢产物触发细胞形状的变化和活性蛋白重组. 脂氧原酶和环氧原酶途径介导着不同的动因事件,揭示了一个新的信号机制.
科学领域:
- 细胞生物学 细胞生物学
- 生物化学 生物化学
- 分子信号传输的方法
背景情况:
- 皮表皮生长因子 (EGF) 诱导了显著的细胞形态变化,包括动蛋白聚合和应力纤维分解.
- 连接EGF受体氨酸激酶活性与细胞骨重组的精确分子机制尚不清楚.
- 最近已经确定了阿拉基酸代谢物作为EGF信号传导的参与者.
研究的目的:
- 阐明阿拉基酸代谢物在介导EGF诱导的细胞骨变化的作用.
- 在EGF信号传递中区分脂氧酶和环氧氧酶途径的贡献.
- 了解EGF引起的细胞圆化背后的机制.
主要方法:
- 在A431细胞,HeLa细胞和老鼠-1纤维细胞中研究了EGF诱导的actin聚合和应力纤维分解.
- 通过使用特定的抑制剂或通过分析代谢物产生来评估氧化酶和环氧化酶途径的参与.
- 监测了依赖于EGF的细胞形态变化,特别是细胞圆形化.
主要成果:
- 由EGF诱导的皮质活性聚合是由脂氧基酶代谢的介导.
- EGF诱导的压力纤维分解是由循环氧化酶代谢产物介导的.
- 在A431细胞中由EGF引起的细胞圆化取决于酸代谢.
结论:
- 在EGF信号传导中,白细胞和前列腺素协同作为第二信使.
- 这些代谢物协调形态效应和actin重组.
- 这项研究揭示了一种新的生长因子诱导的细胞骨变化的机制.
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