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miRNA-126 enhances viability, colony formation, and migration of keratinocytes HaCaT cells by regulating PI3 K/AKT signaling pathway

机译:MiRNA-126通过调节PI3 K / AKT信号通路来增强活力,菌落形成和角质形成细胞HaCAT细胞的迁移

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摘要

Wound healing is a basic biological process including proliferation and migration of keratinocyte. The effects of microRNAs on skin wound healing remain largely unexplored. This study aimed to investigate the role of microRNA-126 (miR-126) in human skin wound healing. Relative expression of miR-126 after injury was evaluated by qRT-PCR. Cell viability, colony formation, cycle distribution, migration, and the alternation of PI3 K/AKT pathway after miR-126 knockdown or overexpression were detected, respectively. In addition, potential target gene of miR-126 was also explored by luciferase assay. Results showed that miR-126 was up-regulated during skin wound healing. Moreover, overexpression of miR-126 promoted cell proliferation and migration, whereas inhibition of miR-126 led to the opposite effects. Additionally, we discovered that PLK2, which inhibited cell viability, colony formation and migration of keratinocyte, was a target gene of miR-126. The expression of PLK2 was negatively correlated with the level of miR-126 during wound healing. Finally, we demonstrated that overexpression of miR-126 significantly increased the expression of p-AKT, p-ERK2, and PI3 K, indicating that overexpression of miR-126 activated PI3 K/AKT signaling pathway. In conclusion, our results demonstrated that miR-126 acted as a critical regulator for promoting proliferation and migration in keratinocyte during skin wound healing.
机译:伤口愈合是一种基本的生物过程,包括角质形成细胞的增殖和迁移。 MicroRNA对皮肤伤口愈合的影响仍然很大程度上是未开发的。本研究旨在探讨MicroRNA-126(miR-126)在人体皮肤伤口愈合中的作用。通过QRT-PCR评估损伤后miR-126的相对表达。分别检测细胞活力,菌落形成,循环分布,迁移和MiR-126敲低或过表达后PI3 k / akt途径的交替。此外,荧光素酶测定还探讨了miR-126的潜在靶基因。结果表明,在皮肤伤口愈合期间miR-126上调。此外,MIR-126的过表达促进了细胞增殖和迁移,而MIR-126的抑制导致相反的效果。另外,我们发现PLK2抑制细胞活力,菌落形成和角质形成细胞的迁移是miR-126的靶基因。 PLK2的表达与伤口愈合期间miR-126的水平负相关。最后,我们证明MiR-126的过表达显着增加了p-Akt,p-Erk2和Pi3 k的表达,表明MiR-126活化的PI3 k / akt信号传导通路的过度表达。总之,我们的结果表明,MIR-126作为临时调节剂,用于在皮肤伤口愈合期间促进角质形成细胞的增殖和迁移。

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