评估酸盐诱导的皮肤细胞衰老的潜在分子机制
Sufei Du1, Fan Yang1, Liping Wu1
1Key Laboratory of Environmental Pollution Monitoring and Disease Control, Ministry of Education & School of Public Health, Guizhou Medical University, Dongqing Road 2, Guiyang 550025, China.
Toxicology research
|November 2, 2023
概括
暴露会通过ERK/CEBPB通路引起皮肤细胞衰老. 激活这种途径促进衰老,而抑制它减少损伤,提供潜在的治疗点.
科学领域:
- 环境健康 环境健康
- 细胞生物学 细胞生物学
- 皮肤病学 皮肤病学
背景情况:
- 暴露是与皮肤损伤相关的全球健康问题.
- 细胞衰老与引起的皮肤损伤有关,ERK/CEBPB通路是潜在的调解者.
- 在诱导的皮肤细胞衰老中,这种途径的确切机制尚不清楚.
研究的目的:
- 阐明ERK/CEBPB信号通路在诱导的HaCaT细胞衰老中的作用和机制.
- 研究如何操纵ERK和CEPB影响诱导的皮肤细胞衰老.
主要方法:
- 基因工程被用来创建稳定的HaCaT细胞系.
- 进行了ERK和CEPBB的淘汰和过度表达,以评估通路活性.
- 分析了细胞衰老标记,细胞循环停止和SASP分泌.
主要成果:
- 抑制CEPB或ERK降低了ERK/CEBPB通路的调节,减少了引起的皮肤细胞衰老.
- 过度表达CEBPB或ERK上调了该途径,加剧了引起的皮肤细胞衰老.
- 酸激活了ERK/CEBPB通路,促进了SASP分泌和p53,p21和p16的表达,导致细胞循环停止和衰老.
结论:
- 该ERK/CEBPB信号通路是诱导的皮肤细胞衰老的关键媒介.
- 针对ERK/CEBPB通路可能提供一种策略,以减轻引起的皮肤损伤.
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