乳腺纤维细胞在对电离辐射的反应中通过细胞外囊泡分泌损伤相关的分子模式
bioRxiv : the preprint server for biology
|December 15, 2025
概括
电离辐射 (IR) 暴露导致乳腺纤维细胞释放更多的细胞外囊泡 (EV). 这些EV携带与损伤相关的分子模式 (DAMP),可能在放射治疗后导致炎症.
科学领域:
- 辐射瘤学 辐射瘤学
- 细胞生物学 细胞生物学
- 辐射伤害的分子机制
背景情况:
- 电离辐射 (IR) 是癌症治疗的基石,诱导细胞死亡和衰老.
- 红外线造成的组织损伤涉及与损伤相关的分子模式 (DAMP) 引发炎症.
- 细胞外囊泡 (EVs) 和DAMP释放在辐射损伤中的作用尚未完全理解.
研究的目的:
- 为了研究DAMP释放和EV分泌在IR之后的机制.
- 为了描述由IR暴露的细胞分泌的EVs的货物.
- 探索特定蛋白质在红外诱导的EV分泌中的作用.
主要方法:
- 在乳腺纤维细胞中诱导急性红外损伤.
- 分析细胞表型和EV分泌率.
- 在电动汽车上进行定量蛋白质组分析.
- 使用GTPase Rab27a.的基因淘汰.
主要成果:
- 急性IR诱导了类似衰老的表型,并在乳腺纤维细胞中增加了EV分泌.
- 红外诱导的EV被增添了DAMP和促炎媒介.
- 敲除Rab27a减少了IR诱导的EV分泌和EV中的DAMP丰富.
结论:
- EVs在IR后调解炎症反应中发挥着重要作用.
- 与EV相关的蛋白质是细胞对辐射损伤反应的关键调解者.
- Rab27a对于IR诱导的EV分泌和DAMP负荷至关重要.
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