电场通过通过PI3K/AKT/Snail通路向下调节E-cadherin来逆转质细胞单层的分化
Chao Wu1, Xu Chen1, Wanqi Huang1
1Department of Plastic Surgery, State Key Laboratory of Trauma and Chemical Poisoning, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing, 400038, China.
Heliyon
|July 18, 2024
概括
电场 (EFs) 通过减少角质细胞分化,促进皮肤伤口愈合. EFs通过PI3K/AKT/Snail通路降低E-cadherin的表达,增强状细胞的迁移和重新表皮化.
科学领域:
- 细胞生物学 细胞生物学
- 皮肤病学 皮肤病学
- 生物物理学的生物物理.
背景情况:
- 重新上皮质化对于皮肤伤口愈合至关重要,涉及状细胞的迁移,增殖和分化.
- 已知内源电场 (EFs) 可以促进表皮的迁移到伤口中心,但根本的机制尚不清楚.
研究的目的:
- 阐明电场 (EF) 在伤口愈合过程中影响状细胞分化和迁移的分子机制.
- 研究E-cadherin和PI3K/AKT/Snail通路在EFs介导的角质细胞反应中的作用.
主要方法:
- 在体外研究中,使用暴露于EFs的培养式皮细胞单层.
- 基因操纵 (Snail knockdown) 和药物抑制 (PI3K 抑制剂 LY294002) 的方法.
- RNA测序和KEGG通路分析.
- 在生体内使用猪全厚皮肤伤口模型进行的研究.
主要成果:
- EFs的应用逆转了角质细胞分化,由减少的K1和K10表达体现出来.
- 通过抑制PI3K/AKT/Snail信号通路,EFs降低了E-cadherin的表达.
- 在体内,弱化的内源EF导致了E-cadherin的增加和新形成的表皮的早期分化.
结论:
- 电场 (EF) 通过通过PI3K/AKT/Snail路径减少E-cadherin表达来促进伤口再上皮化,从而减少角质细胞的分化和增强迁移能力.
- 这项研究揭示了EFs在调节角质细胞行为的新机制,并提供了优化伤口愈合策略的见解.
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