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在缺氧缺血症条件下,LOX-1通过p38-MAPK/NF-κB通路调解微质细胞的炎症激活

Yoshinori Aoki^1,2,3, Hongmei Dai¹, Fumika Furuta¹

¹Department of Mental Retardation and Birth Defect Research, National Institute of Neurology, National Center of Neurology and Psychiatry, Kodaira, Tokyo, Japan.

Cell communication and signaling : CCS

|June 2, 2023

概括

缺氧和缺血诱导微质细胞中类似莱克的氧化低密度脂蛋白受体-1 (LOX-1),激活炎症反应. 准LOX-1为大脑免疫系统激活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
分子生物学分子生物学

背景情况:

微质细胞是大脑免疫系统的关键参与者,表现出有害和保护性的作用.
乳素类氧化低密度脂蛋白受体-1 (LOX-1) 表达在新生儿缺氧性缺血性脑病变 (nHIE) 的病理病变内的微细胞中升高.
LOX-1通过细胞内信号通路作为细胞因子和化学因子的激活剂.

研究的目的:

在低氧和缺血条件下研究LOX-1在微质细胞中的新型作用.
在这些条件下阐明在微质细胞中控制LOX-1基因转录的分子机制.

主要方法:

小鼠初级微质细胞被分离出来,并作为一个体外 nHIE 模型,接受氧气-葡萄糖剥夺 (OGD).
评估了LOX-1,细胞因子和化学因子的表达水平,包括和没有siRNA和抑制剂.
使用露西法酶记者和染色体免疫沉降试验来确认转录因子与OLR-1基因促进体结合.

主要成果:

氧气和营养缺乏触发了LOX-1的表达,导致炎症媒介 (IL-1β,IL-6,TNF-α,CCL2,CCL5,CCL3) 和活性氧/物种的释放.
抑制LOX-1,p38-MAPK和NF-κB通路可以抑制炎症媒介的产生.
NF-κB和HIF-1α被确定为与OLR-1基因促进体结合的转录因子,NF-κB显示出显著的转录活性.
在微质细胞中通过细胞内LOX-1通路内的正反循环观察到LOX-1过度表达的自调节.

结论:

微质细胞中的缺氧/缺血状况诱导LOX-1表达,随后激活大脑的免疫系统.
LOX-1及其相关分子在涉及微质激活和神经炎症的疾病中代表着有前途的治疗点.

关键词:

氧气过低是因为缺氧.缺血缺血是因为缺血.洛克斯-1号机场微质细胞中的微质细胞 NF-卡帕B (NF-κB) 是一个在OLR-1中,OLR-1是OLR-1.在p38-MAPKK中使用.

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