小胶质细胞
细胞凋亡
细胞生物学
受体
一氧化氮合酶
炎症
医学
一氧化氮
免疫学
分子生物学
生物
内科学
生物化学
作者
Jian-Wu Ni,Caixia Li,Xiongwei Chen,Wenpin Cai
出处
期刊:Neurology India
[Medknow Publications]
日期:2022-01-01
卷期号:70 (6): 2378-2378
被引量:2
标识
DOI:10.4103/0028-3886.364080
摘要
Microglia play a crucial role in the activation of immune defense mechanism as the resident macrophages in the central nervous system (CNS). Microglia can eliminate damaged neurons, plaques, and other infectious agents. Triggering receptor expressed on myeloid cell-2 (TREM-2) speculates to be beneficial in preventing inflammation-induced bystander damage of neurons. However, the precise molecular mechanisms underlying the regulation of TREM-2 on neurons are not clarified. We cultured PC12 cells with conditioned medium which was the supernatant of LPS-treated BV2 cells and six groups of PC12 cells (control group, LPS group, TREM-2 WT + LPS group, TREM-2 over-expression + LPS group, siRNA control + LPS group, and siRNA TREM-2 + LPS group) were investigated. The mRNA levels of inflammatory mediators: Nitric oxide synthase (iNOS) and Arginase-1(Arg-1) were quantified by using RT-PCR. Assessment of apoptosis in PC12 cells mediated by BV2 microglia was analyzed using TUNEL assays. The result showed that LPS stimulation significantly enhanced inducible iNOS (M1) production in BV2 cells (P < 0.01), and increased PC12 cells apoptosis (P < 0.01), while reduced the production of Arg-1 (M2) in BV2 cells (P < 0.01). These effects were attenuated by TREM-2 over-expression, but enhanced by TREM-2 silencing. It indicated that TREM-2 inhibited LPS-mediated neuronal apoptosis by down-regulating iNOS and up-regulating the expression of Arg-1 in BV2 microglia. Therefore, our findings may provide new insights in the regulation of TREM-2 on neuronal apoptosis via BV2 microglial M1/M2 modulation.
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