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首页> 外文期刊>Journal of cellular biochemistry. >Migration of F9 parietal endoderm cells is regulated by the ERK pathway.
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Migration of F9 parietal endoderm cells is regulated by the ERK pathway.

机译：F9壁层内胚层细胞的迁移受ERK途径调控。

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摘要

Cell migration is regulated by the action of many signaling pathways that are activated in specific regions of migrating cells. Extracellular regulated kinase 1/2 (ERK) signaling can modulate the migration of cells by controlling the turnover of focal adhesions and the dynamics of actin polymerization. Focal adhesion turnover is necessary for cell migration, and the formation of strong actin stress fibers and mature focal adhesions puts the brakes on cell migration. We used F9 wild-type and vinculin null (vin-/-) parietal endoderm (PE) outgrowth to study the role of the ERK signaling pathway in cell migration. Upon plating of F9 embryoid bodies (EBs) onto laminin-coated dishes, PE cells migrate away from the EBs, providing an in vitro model for studying directed migration of this embryonic cell type. Our results suggest that the ERK pathway regulates PE cell migration by affecting the formation of focal adhesions and lamellipodia through the action of myosin light chain kinase (MLCK).
机译：细胞迁移受迁移细胞特定区域中激活的许多信号通路的调控。细胞外调节激酶1/2（ERK）信号传导可通过控制粘着斑的转换和肌动蛋白聚合的动力学来调节细胞的迁移。局灶性粘附转换是细胞迁移所必需的，而强大的肌动蛋白应激纤维和成熟的局灶性粘附形成会阻碍细胞迁移。我们使用F9野生型和长春花叶素（vin-/-）顶叶内胚层（PE）增生来研究ERK信号通路在细胞迁移中的作用。将F9胚状体（EB）铺在层粘连蛋白包被的培养皿上后，PE细胞会从EB迁移，从而为研究这种胚细胞类型的定向迁移提供了体外模型。我们的结果表明，ERK途径通过肌球蛋白轻链激酶（MLCK）的作用来影响粘着斑和片状脂膜的形成，从而调节PE细胞的迁移。

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