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首页> 外文期刊>Molecular biology of the cell >Erk5 Controls Slug Expression and Keratinocyte Activation during Wound Healing
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Erk5 Controls Slug Expression and Keratinocyte Activation during Wound Healing

机译：伤口愈合过程中Erk5控制子弹头表达和角质形成细胞活化。

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摘要

Reepithelialization during cutaneous wound healing involves numerous signals that result in basal keratinocyte activation, spreading, and migration, all linked to a loosening of cell-cell adhesion structures. The transcription factor Slug is required for this process, and EGF treatment of human keratinocytes induced activating phosphorylation of Erk5 that coincides with slug transcription. Accordingly, ectopic activation of Erk5 led to increased Slug mRNA levels and faster wound healing, whereas keratinocyte migration was totally blocked by Erk5 pathway inhibition. Expression of a shRNA specific for Erk5 strongly diminished Erk5 levels in keratinocytes and significantly decreased their motility response to EGF, along with induction of Slug expression. These Erk5-deprived keratinocytes showed an altered, more compact morphology, along with disruption of desmosome organization. Accordingly, they displayed an altered ability to form cell aggregates. These results implicate a novel EGFR/Erk5/Slug pathway in the control of cytoskeleton organization and cell motility in keratinocytes treated with EGF.
机译：皮肤伤口愈合过程中的上皮再生涉及许多信号，这些信号导致基底角质形成细胞活化，扩散和迁移，所有这些信号都与细胞-细胞粘附结构的松动有关。转录因子Slug是该过程所必需的，并且人角质形成细胞的EGF处理诱导了与Slug转录一致的Erk5的活化磷酸化。因此，Erk5的异位激活导致增加的Slug mRNA水平和更快的伤口愈合，而角质形成细胞的迁移则完全被Erk5途径抑制所阻断。对Erk5特异的shRNA的表达可大大降低角质形成细胞中Erk5的水平，并显着降低其对EGF的运动反应，并诱导Slug表达。这些剥夺了Erk5的角质形成细胞表现出改变的，更紧凑的形态，以及对桥粒组织的破坏。因此，它们显示出形成细胞聚集体的能力改变。这些结果暗示了在用EGF处理的角质形成细胞的细胞骨架组织和细胞运动控制中的新型EGFR / Erk5 / Slug途径。

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