首页> 中文期刊> 《中南大学学报(医学版)》 >黏着斑激酶对ERK介导的滋养层细胞侵袭行为的调节作用

黏着斑激酶对ERK介导的滋养层细胞侵袭行为的调节作用

         

摘要

目的:探讨黏着斑激酶(FAK)在细胞外信号调节激酶(extracellular signal-regulated kinase,ERK)信号通路介导的滋养层细胞侵袭中的作用.方法:利用人绒毛外细胞滋养层(extravillous cytotrophoblasts,EVCT)细胞体外侵袭模型,加入不同浓度的黏着斑激酶抑制剂herbimycin A和ERK抑制剂PD98059,观察其对滋养层细胞生长的影响,FAK,ERK磷酸化的影响以及对滋养层细胞侵袭能力的影响.结果:Herbimycin A呈浓度依赖方式抑制EVCT细胞中磷酸化FAK的表达; herbimycin A能够部分抑制磷酸化ERK1/2表达,而PD98059对磷酸化FAK的表达未见影响;herbimycin A,PD98059均能不同程度地抑制EVCT细胞的体外侵袭作用.结论:ERK信号通路可能是多种侵袭信号的共同通路,其在滋养层细胞侵袭行为调节中起重要作用.%Objective To investigate the role of focal adhesion kinase (FAK) in extraeellular signal-regulated kinase (ERK) signaling pathway mediated invadsion of trophoblasts. Methods We established a human extravillous cytotrophoblasts in vitro invasion model. Different concentrations of herbimycin A( FAK inhibitor)and PD98059 (ERK inhibitor) were given to observe the influence on the growth of trophoblast cells, FAK, ERK phosphorylation, and trophoblast invasion abilities. Results The expression of phosphorylated FAK in the extravillous cytotrophoblasts (EVCT) was inhibited by herbimycin A in a concentration-dependent manner and expression of phosphorylated ERK1/2 was also partially reduced. PD98059 had no effect on the expression of phosphorylated FAK. Herbimycin A and PD98059 suppressed the in vitro invasion of EVCT to various degrees. Conclusion ERK signaling pathway may be the common pathway for many invasive signals, and play a key role in the regulation of trophoblast invasion.

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