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M2a巨细胞调节纤维化,并通过纤维细胞中的PU.1/mTOR通路影响中风后的结果

Jiagui Huang¹, Yue Chen², Li Zhou²

¹Department of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China; Department of Neurology, The Second People's Hospital of Yibin, Yibin, China.

Neurochemistry international

|January 6, 2024

概括

M2a巨细胞通过在纤维细胞中调节PU.1来促进中风后纤维化,从而影响功能恢复. 这通过PU.1/mTOR途径发生,影响痕形成和神经结果.

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:

纤维性痕形成对于中风后的功能恢复至关重要.
在脑缺血后,M2a巨细胞有助于早期纤维化.
在中风中巨细胞纤维细胞相互作用的机制尚不清楚.

研究的目的:

在缺血性中风中调查巨细胞纤维细胞相互作用.
阐明M2a巨细胞在中风引起的纤维化中的作用.
确定参与M2a巨介导纤维化的分子途径.

主要方法:

使用M2a巨受条件介质 (MCM) 的体外和体内研究.
在纤维细胞中操纵PU.1表达和mTOR信号.
在老鼠中,中脑动脉封闭/再输 (MCAO/R) 模型.
介质素-4 (IL4) 的使用可诱导M2a两极化.

主要成果:

M2a MCM上调了纤维细胞PU.1的表达,促进了分化,增殖,迁移和细胞外矩阵的产生.
在体内IL4治疗增强了PU.1表达,纤维化,血管新生和MCAO/R后的神经恢复.
IL4增加了酸化Akt和mTOR;PU.1敲击逆转了这些影响.
抑制mTOR抑制了纤维细胞迁移,分化和原蛋白合成.

结论:

M2a巨细胞通过纤维细胞中的PU.1/mTOR信号通路调节中风后纤维化.
这一途径影响纤维细胞的行为和细胞外基质的产生.
准PU.1/mTOR通路可能为中风恢复提供治疗策略.

关键词:

纤维母细胞细胞是如何形成的纤维性痕是一个纤维性痕.缺血性中风是因为缺血性中风.巨细胞是一个巨细胞.中脑动脉封闭/再输血在PU.1中,PU.

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