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来自缺氧血管光滑肌肉细胞的外体SRC通过促进M1微质极化来加剧缺血性脑损伤

Xiaoting Zhang¹, Jingpei Guo¹, Junbin Liu¹

¹Center of Interventional Medicine, The Fifth Affiliated Hospital of Sun Yat-sen University, Zhuhai, Guangdong Province, 519000, China; Center of Cerebrovascular Disease, The Fifth Affiliated Hospital of Sun Yat-sen University, Zhuhai, Guangdong Province, 519000, China; Guangdong Provincial Engineering Research Center of Molecular Imaging, The Fifth Affiliated Hospital, Sun Yat-sen University, Zhuhai, Guangdong Province, 519000, China.

Neurochemistry international

|July 31, 2024

概括

缺氧血管光滑肌细胞外体促进M1微质激活,恶化缺血性中风 (IS) 脑损伤. 在这些外体中抑制Src,通过减少炎症和保护神经元,为IS提供了潜在的治疗策略.

科学领域:

神经科学是一个神经科学.
免疫学免疫学免疫学
细胞生物学细胞生物学

背景情况:

炎症性M1微质细胞在缺血性中风 (IS) 后恶化脑损伤.
血管光滑肌细胞 (VSMCs) 在缺血条件下分泌出外体.
外体调节微质极化,影响炎症反应.

研究的目的:

研究由低氧VSMCs (HExos) 衍生出的外体在微质极化和IS中的作用.
确定潜在的治疗目标,以减轻IS引起的脑损伤.

主要方法:

从正常性 (Exos) 和低氧性 (HExos) 的人类VSMC中分离和表征外体.
与人类初级微质细胞 (HM1900) 共同化HExos以评估M1极化.
对HExos的蛋白质组分析以确定关键介质 (例如Src).
在体外和体内 (pMCAO小鼠模型) 实验中使用Src抑制剂达斯atinib (DAS).

主要成果:

HExos,但不是Exos,在HM1900中显著促进了M1极化.
在HExos中丰富了Src蛋白,并在微质中调节了M1标记物.
达沙替尼 (DAS) 抑制了M1极化,促进了M2表型,减少了M1微质/巨细胞,保护了神经元,并改善了pMCAO小鼠的功能.

结论:

缺氧VSMC衍生的外体通过Src传输促进M1微质极化,有助于后IS炎症.
用达萨提尼布等药物向Src抑制是治疗缺血性中风脑损伤的有希望的治疗策略.

关键词:

达沙替尼布 (Dasatinib) 是一种缺血性中风是因为缺血性中风.微质的极化是微质的极化美国Src Src 血管光滑肌肉细胞衍生的外体细胞.

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