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来自M2巨细胞的细胞外囊泡通过通过miR221-5p调节巨细胞极化来保护腹腔大动脉动脉瘤

Yang Ma^1,2, Xiang-Jiu Ding^3,4, Si-Yu Lu^1,2

¹Department of Critical Care Medicine, Qilu Hospital of Shandong University, No. 107, Wen Hua Xi Road, Jinan, 250012, Shandong, China.

Cellular & molecular biology letters

|August 10, 2025

概括

来自M2巨细胞的细胞外囊泡 (EVs) 通过输送miR221-5p来防止腹腔大动脉动脉瘤 (AAA). 这种微RNA通过PARP-1/PP-1ɑ/JNK/c-Jun通路调节巨细胞极化,为AAA提供了潜在的治疗策略.

科学领域:

心血管生物学心血管生物学
血管生物学血管生物学
细胞外囊泡研究研究

背景情况:

来自M2巨细胞 (M2-EVs) 的细胞外囊泡 (EVs) 已知在急性肺损伤中起着保护作用.
在腹腔大动脉动脉瘤 (AAA) 中M2-EVs的特定功能和潜在机制在很大程度上仍未被探索.

研究的目的:

研究M2-EVs在腹腔大动脉动脉瘤 (AAA) 发病过程中的作用和治疗潜力.
阐明M2-EVs在AAA中发挥其作用的分子机制,重点关注微RNA参与.

主要方法:

从M2巨细胞中提取了M2-EVs,这些巨细胞被miR221-5p反感性寡核酸 (ASOs) 刺激,并给ApoE-/-小鼠服用血管新生素II诱导的AAA.
试验室研究涉及与人类大动脉内皮细胞 (HAEC) 共同培养初级骨髓衍生单细胞 (BMDMs),以评估M2-EVs对氧化应激和炎症的影响.
在M2-EV和AAA组织上进行了RNA测序,以确定关键的分子参与者,机械学研究探索了PARP-1/PP-1ɑ/JNK/c-Jun信号通路.

主要成果:

在小鼠中,M2-EV的使用显著降低了AAA发生率,大动脉直径和巨细胞透,同时改善了血管完整性和α-SMA表达.
RNA测序确定了miR221-5p在M2-EVs上调和AAA下调;通过ASO抑制miR221-5p降低了M2-EVs的保护作用.
通过miR221-5p/PARP-1/PP-1ɑ/JNK/c-Jun通路,M2-EVs促进了M2巨细胞的两极分化,并缓解了HAEC中的氧化应激和炎症.

结论:

在M2-EVs中的miR221-5p是AAA病理生理学中的关键调解者,通过PARP-1/PP-1ɑ/JNK/c-Jun信号级联调节巨细胞极化.
M2-EV及其封装的miR221-5p作为治疗腹腔大动脉瘤治疗的新疗法具有显著的前景.

关键词:

腹腔大动脉动脉瘤腹腔大动脉动脉瘤细胞外囊泡中的细胞外囊泡.在M2巨细胞中.巨细胞的两极分化微型RNA 221-5p 是一个微型RNA.

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