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通过高葡萄糖刺激皮肤细胞的KRT17促进了角质细胞的增殖和迁移

Peng Zhou¹, Haijun Feng², Wenhui Qin³

¹Department of Vascular Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.

Frontiers in endocrinology

|November 6, 2023

概括

在高葡萄糖条件下的氨酸17 (KRT17) 上调会通过通过c-MYB/PI3K-AKT通路促进氨酸细胞的增殖和迁移,从而损害糖尿病伤口愈合. 沉默KRT17改善了糖尿病小鼠的愈合.

科学领域:

生物化学生化学
细胞生物学细胞生物学
皮肤病学皮肤病学

背景情况:

糖尿病患者的伤口愈合显著受损,角质细胞的增殖和迁移对于皮肤修复至关重要.
超化是已知的因素,可以阻碍糖尿病患者的伤口愈合速度.

研究的目的:

研究素17 (KRT17) 在糖尿病伤口愈合中的作用.
阐明KRT17影响状细胞行为和伤口修复的分子机制.

主要方法:

建立了一个体外细胞模型,使用KRT17刺激的人类不朽化角质细胞 (HaCaT) 细胞.
使用db/db小鼠模型评估KRT17沉默对糖尿病伤口愈合的影响.
进行了转录组测序 (RNA-seq) 和体外检测,以分析分子通路和蛋白质表达.

主要成果:

在体外,KRT17刺激促进了角质细胞的增殖和迁移.
在db/db小鼠模型中,KRT17沉默加速了糖尿病伤口愈合.
KRT17上调了c-MYB mRNA和增强了PI3K-AKT通路活性,包括增加了c-MYB表达和pAKT水平.

结论:

在高葡萄糖条件下,KRT17的调节升高,导致高胆固醇症和糖尿病伤口愈合的延迟.
KRT17通过c-MYB/PI3K-AKT信号通路促进了角质细胞的增殖和迁移.
准KRT17可能是改善糖尿病伤口愈合的治疗策略.

关键词:

这些细胞是Hacat细胞.Krt1717 在线观看糖尿病患者的伤口愈合移民移民迁移迁移它们的扩散和扩散.

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