巨细胞迁移抑制因子通过与胺相关的蛋白质1介导的自活性激活加剧了喘性气道重塑
Jin Liu1, Yuqian Chen1, Huan Chen1
1Department of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Xi'an Jiaotong University, No. 277, West Yanta Road, Xi'an, Shaanxi, 710061, People's Republic of China.
Respiratory research
|September 6, 2023
概括
巨细胞迁移抑制因子 (MIF) 通过激活自和通过ERK/Drp1通路降解E-cadherin促进喘. 针对这种途径可能会提供新的喘治疗方法.
科学领域:
- 细胞生物学 细胞生物学
- 免疫学 免疫学 免疫学
- 呼吸系统医学 呼吸系统医学
背景情况:
- 巨细胞迁移抑制因子 (MIF) 和异常的线粒体裂变都与喘病因产生有关.
- 在MIF诱导的气道平滑肌细胞增殖和气道重塑中,DRp1介导的线粒体裂变的确切作用尚不清楚.
研究的目的:
- 阐明DRp1介导的线粒体裂变及其下游目标在MIF诱导的气道平滑肌细胞增殖和慢性喘气道改造中的作用.
主要方法:
- 使用初级培养的呼吸道光滑肌细胞 (ASMC) 和卵胺 (OVA) 诱导的喘大鼠模型.
- 检测包括CCK-8,EDU,西式抹杀,传输电子显微镜和组织学染色.
- 评估了细胞增殖,信号通路 (ERK1/2,Drp1),自,E-cadherin表达和喘发育标志物.
主要成果:
- MIF激活了ERK1/2,导致了Drp1酸化,增强了自,并减少了E-cadherin,促进了ASMC的扩散.
- 在喘大鼠中,MIF抑制,线粒体分裂抑制或自抑制减弱了呼吸道重塑.
结论:
- 通过ERK/Drp1信号通路激活自和E-cadherin降解,MIF促进了喘气道的重塑.
- 准MIF/ERK/Drp1通路为喘预防和治疗提供了潜在的治疗策略.
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