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circ_0000554促进巨细胞M2两极分化通过糖质重编程的介导,并加剧COPD损伤

Yamei Song¹, SiQin Han², Linlin Liu³

¹The First Department of Pulmonary and Critical Care Medicine, The Second Hospital of Hebei Medical University, 215 Heping West Road, Shijiazhuang, Hebei 050000, China; Department of Pulmonary and Critical Care Medicine, Harrison International Peace Hospital, 180Renmin East Road, Hengshui, Hebei 053000, China.

Toxicology letters

|June 24, 2025

概括

细颗粒物 (PM2.5) 暴露加剧慢性阻塞性肺病 (COPD) 通过促进M2巨细胞的两极分化. 这个过程是由循环RNA hsa_circ_0000554 介导的,它激活SLC2A3表达,恶化肺损伤.

科学领域:

环境健康环境健康
肺部病理学肺部病理学
分子生物学分子生物学

背景情况:

环境污染,特别是细颗粒物 (PM2.5) 严重影响人类健康,尤其是慢性阻塞性肺病 (COPD) 的恶化.
在PM2.5诱导的COPD病原体背后的精确炎症机制尚未完全理解.
循环RNAs (circRNAs) 和巨细胞两极分化越来越被认为是COPD发展的关键因素.

研究的目的:

为了研究hsa_circ_0000554在PM2.5引起的COPD中的作用.
阐明涉及circRNAs,巨细胞两极分化和COPD炎症的调节途径.
确定潜在的治疗目标,以减轻PM2.5相关的COPD恶化.

主要方法:

对GEO数据库 (GSE150251) 的选,以确定暴露于PM2.5.5的COPD患者中差异表达的circRNA.
在实验室模型中,使用用IL-4和PM2.5.5治疗的膜巨细胞 (MH-S) 进行实验.
流细胞测量和RT-qPCR用于评估巨细胞极化和基因表达.
生物信息学预测和分子生物学测试以确定hsa_circ_0000554,miR-548b-3p和SLC2A3.3之间的相互作用.
在动物模型中进行体内验证.

主要成果:

在COPD患者和在PM2.5暴露后的体外模型中,Hsa_circ_0000554显著上调.
PM2.5诱导了膜巨细胞的M2型极化,这在COPD炎症中起着关键作用.
发现Hsa_circ_0000554针对miR-548b-3p,调节溶性载体家族2成员3 (SLC2A3) 的表达.
通过代谢重编程,PM2.5促进M2巨细胞的两极分化,由circ_0000554介导的SLC2A3表达激活,最终恶化COPD损伤.

结论:

Hsa_circ_0000554是PM2.5诱导的COPD病原发生的关键媒介.
在circ_0000554/miR-548b-3p/SLC2A3轴驱动M2巨细胞的极化和炎症,以响应PM2.5.5.
针对这种途径可能为管理PM2.5相关的慢性肺炎提供一种新的治疗策略.

关键词:

慢性阻塞性肺病是一种慢性阻塞性肺病.圆周_0000554 在线观看微细颗粒物质的细颗粒物质的细颗粒物质的细颗粒物质.巨细胞是一个巨细胞.代谢重编程是一种代谢重编程.

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