| 韩秀敏1 于卉影2 孙英慧2 朱鲜阳1 张坡1 崔春生1.Rac1/MAPK/ERK 通路介导脂多糖LPS 诱导的人内皮细胞
单层通透性增高机制研究[J].现代生物医学进展英文版,2012,12(9):1609-1612. |
| Rac1/MAPK/ERK 通路介导脂多糖LPS 诱导的人内皮细胞
单层通透性增高机制研究 |
| LPS Regulates the Enhancement of HUVEC PermeabilityMediatedby Rac1- MAPK/ERK Signal Pathway |
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| DOI： |
| 中文关键词: LPS HUVEC Rac1 ERK 通透性 |
| 英文关键词: LPS HUVEC Rac1 ERK Permeability |
| 基金项目:辽宁省科技攻关计划资助项目（2005225013-15） |
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| 中文摘要: |
| 目的：探讨LPS 诱导的人内皮细胞单层通透性改变的分子机制。方法：应用逆转录病毒为载体，感染并筛选稳定表达持续活
化型Rac1 和主导抑制型Rac1 的人HUVEC 细胞，应用LPS 刺激并观察细胞骨架蛋白F-actin 和HUVEC 单层通透性的改变。同
时应用Western blot 方法检测LPS 刺激前后细胞中MAPK/ERK 信号通路的改变及加入PD98059 阻断ERK 表达后，细胞内
F-actin 的改变情况。结果：与正常HUVEC 相比较，LPS 刺激后，感染活化型Rac1 和主导抑制型Rac1 的HUVEC 中F-actin 重构
并形成大量应力纤维，细胞单层通透性显著增加。而抑制型Rac1 感染后的HUVEC 中F-actin 无重构现象，同时细胞单层通透性
无明显增加。LPS 刺激前后，各组细胞中ERK1/2 总蛋白均无明显改变。LPS 刺激后，感染活化型Rac1 的HUVEC 中，p-ERK 增
加。经PD98059 阻断后，细胞内p-ERK 表达下降同时伴随F-actin 解聚发生。结论：LPS 诱导的内皮细胞通透性增加是经过
Rac1-MAPK/ERK 通路介导的。 |
| 英文摘要: |
| Objective: To investigate the mechanism of LPS regulating the enhancement of endothelium permeability in vitro.
Methods: The HUVECs in vitro were infected by the retrovirals mediated domain-negative N17Rac1 and activate Q61Rac1. The increase
of endothelial permeability was induced by addition of LPS and the change of F-actin cytoskeleton was investigated by
phallodin-Rhodamin staining. The expressions of pERK and total ERK were detected by western blot with and without addition of LPS.
Subsequently, F-actin cytoskeleton of HUVEC was investigated by phallodin-Rhodamin staining when cells was incubated by PD98059
to block the activation of pERK. Results: Compared with that in the normal HUVECs, the formation of actin stress fibers was
investigated associated with the enhancement of endothelial permeability in cells infected with Q61Rac1 with and without treatment of
LPS. In contrast, there were no changes in cells infected with N17Rac1. Although there was change in the total ERK1/2 with or without
LPS treatment in HUVECs, the expression of pERK significantly increased in cells treated by LPS by Western blotting. Meanwhile, the
expression of pERK enhance in Q61Rac1-infected HUVECs with or without LPS stimulation. Reversely, the cells infected by N17Rac1
inhbited the activation of pERK induced by LPS. Moreover, when cells were treated with PD98059, a pERK inhibitor, LPS induced
F-actin stress fibre disformated and the endothelial permeability was inhbited in Q61Rac1-infected cells. Conclusion: Rac1-MAPK/ERK
is involved in the regulation of LPS-indcued endothelial permeability and F-actin stress fiber formation. |
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