Suppr超能文献

氨基磷脂是细胞凋亡时信号转导的 TREM2 配体。

Aminophospholipids are signal-transducing TREM2 ligands on apoptotic cells.

机构信息

Department of Genome-based Drug Discovery, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki, 852-8521, Japan.

Unit for Dementia Research and Drug Discovery, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki, 852-8521, Japan.

出版信息

Sci Rep. 2019 May 17;9(1):7508. doi: 10.1038/s41598-019-43535-6.

Abstract

Variants of triggering receptor expressed on myeloid cells 2 (TREM2) are associated with an increased incidence of Alzheimer's disease, as well as other neurodegenerative disorders. Using a newly developed, highly sensitive reporter cell model, consisting of Jurkat T cells stably overexpressing a reporter gene and a gene encoding TREM2DAP12 fusion protein, we show here that TREM2-dependent signal transduction in response to apoptotic Neuro2a cells is mediated by aminophospholipid ligands, phosphatidylserine and phosphatidylethanolamine, which are not exposed on the intact cell surface, but become exposed upon apoptosis. We also show that signal-transducing TREM2 ligands different from aminophospholipids, which appear to be derived from neurons, might be present in membrane fractions of mouse cerebral cortex. These results may suggest that TREM2 regulates microglial function by transducing intracellular signals from aminophospholipids on apoptotic cells, as well as unidentified ligands in the membranes of the cerebral cortex.

摘要

触发受体表达在髓样细胞 2(TREM2)的变异与阿尔茨海默病的发病率增加有关,以及其他神经退行性疾病。使用一种新开发的、高度敏感的报告细胞模型,该模型由稳定过表达报告基因和编码 TREM2DAP12 融合蛋白的 Jurkat T 细胞组成,我们在这里表明,TREM2 依赖性信号转导对凋亡的 Neuro2a 细胞的反应是由氨基磷脂配体,即磷脂酰丝氨酸和磷脂酰乙醇胺介导的,这些配体在完整的细胞膜表面上不暴露,但在凋亡时暴露。我们还表明,信号转导的 TREM2 配体不同于氨基磷脂,这些配体似乎来源于神经元,可能存在于小鼠大脑皮层的膜部分中。这些结果可能表明,TREM2 通过将凋亡细胞上的氨基磷脂的细胞内信号转导,以及大脑皮层膜中的未鉴定配体,来调节小胶质细胞的功能。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/841e/6525155/cef0678e31c4/41598_2019_43535_Fig1_HTML.jpg

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验