通过膜介质器调节SHED诱导的巨细胞极化和可塑性
Azadeh Mohammad-Hasani1, Saeed Mohammadi1, Mohsen Saeidi2
1Stem Cell Research Centre, Golestan University of Medical Sciences, Gorgan, Iran; Department of Molecular Medicine, Faculty of Advanced Medical Technologies, Golestan University of Medical Sciences, Gorgan, Iran.
Tissue & cell
|July 9, 2025
概括
来自人体脱皮叶状牙 (SHED) 的干细胞将炎症性巨细胞重新编程为修复性M2表型. SHED-MSCs降低炎症和氧化应激,突出了它们对相关疾病的治疗潜力.
科学领域:
- 免疫学 免疫学 免疫学
- 干细胞生物学 干细胞生物学
- 再生医学是一种再生医学.
背景情况:
- 来自人体脱皮叶状牙 (SHED) 的干细胞影响巨细胞的两极分化.
- SHED-MSC与巨细胞相互作用的精确机制需要进一步阐明.
研究的目的:
- 为了研究SHED-MSCs和THP-1细胞衍生的巨细胞之间的交叉对话.
- 评估SHED-MSCs对巨细胞可塑性,表型和功能的影响.
主要方法:
- 使用跨井系统,SHED-MSC与M0和M1极化巨细胞间接共同培养.
- 分析巨细胞表面标记物,细胞因子分泌,氧化应激标记物和基因表达通过流细胞计和其他测试.
主要成果:
- SHED-MSCs诱导了对M2巨细胞表型 (CD206+) 的显著转变.
- 与SHED-MSC共同培养增加了抗炎细胞因子 (TGFB2,IL-10) 和减少了促炎细胞因子 (TNF-α,IL-12).
- SHED-MSCs降低了氧化应激标志物 (NO,MDA) 和增强了抗氧化能力 (TAC,SOD,CAT),以及ARG1上调和IL-6R下调.
结论:
- SHED-MSCs具有对膜效应,将炎症性巨细胞重新编程为修复性表型.
- SHED-MSCs恢复了巨细胞的氧化还原稳定,这表明它有可能治疗炎症和与氧化压力相关的疾病.
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