P2Y2受体通过炎症激活的微质中介于通过炎症激活的微质去除死亡细胞
Izumi Hide1, Hiroko Shiraki1, Akihiro Masuda1
1Department of Molecular and Pharmacological Neuroscience, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima 734-8551, Japan.
Journal of pharmacological sciences
|July 31, 2023
概括
炎症性微质细胞通过P2Y2受体去除垂死的细胞,而P2Y2受体则对Axl受体进行上调. 这种机制对于理解中枢神经系统 (CNS) 中微质功能至关重要.
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:
- 微质细胞对于中枢神经系统的平衡至关重要,清除垂死的细胞.
- 功能障碍的微质清除有助于神经退行症在病理条件下.
- 通过炎症性微质细胞去除死亡细胞的机制尚未完全理解.
研究的目的:
- 为了研究通过炎症性微质细胞去除死亡细胞的纯能调节.
- 阐明P2Y2受体在微质细胞化中的作用.
主要方法:
- 主要大鼠微质细胞的实时成像.
- 脂聚糖 (LPS) 刺激以诱导微质激活和细胞死亡.
- 使用苏拉和AR-C118925的P2受体的药理抑制.
- 通过mRNA和细胞表面局部化分析P2Y2受体和Axel表达.
- 评估下游信号通路,涉及富含林的氨酸激酶 (Pyk2).
主要成果:
- 由LPS刺激的微质细胞积极清除垂死的细胞.
- P2受体对抗剂 (suramin,AR-C118925) 抑制了垂死细胞的去除,特别是在LPS刺激的微中.
- LPS诱导P2Y2受体转移到等离子体膜,并增加其mRNA表达.
- LPS上调细胞受体Axl,这种影响取决于P2Y2受体和Pyk2信号传递.
结论:
- 炎症刺激激活了微质中的P2Y2受体.
- 通过P2Y2受体的激活,可以调解死亡细胞的去除,部分原因是通过调节Axl受体.
- 这种纯能信号通路是炎症性微质细胞灭菌的关键机制.
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