CB2 expression in mouse brain: from mapping to regulation in microglia under inflammatory conditions.

IF 9.3 1区医学 Q1 IMMUNOLOGY

Journal of Neuroinflammation Pub Date : 2024-08-19 DOI:10.1186/s12974-024-03202-8

Wanda Grabon, Anne Ruiz, Nadia Gasmi, Cyril Degletagne, Béatrice Georges, Amor Belmeguenai, Jacques Bodennec, Sylvain Rheims, Guillaume Marcy, Laurent Bezin

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Abstract

Since its detection in the brain, the cannabinoid receptor type 2 (CB2) has been considered a promising therapeutic target for various neurological and psychiatric disorders. However, precise brain mapping of its expression is still lacking. Using magnetic cell sorting, calibrated RT-qPCR and single-nucleus RNAseq, we show that CB2 is expressed at a low level in all brain regions studied, mainly by few microglial cells, and by neurons in an even lower proportion. Upon lipopolysaccharide stimulation, modeling neuroinflammation in non-sterile conditions, we demonstrate that the inflammatory response is associated with a transient reduction in CB2 mRNA levels in brain tissue, particularly in microglial cells. This result, confirmed in the BV2 microglial cell line, contrasts with the positive correlation observed between CB2 mRNA levels and the inflammatory response upon stimulation by interferon-gamma, modeling neuroinflammation in sterile condition. Discrete brain CB2 expression might thus be up- or down-regulated depending on the inflammatory context.

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小鼠大脑中 CB2 的表达：从绘图到炎症条件下小胶质细胞的调节。

自从在大脑中发现大麻素受体 2 型（CB2）以来，它一直被认为是治疗各种神经和精神疾病的有希望的靶点。然而，目前仍缺乏对其表达的精确脑图谱。利用磁性细胞分选、校准 RT-qPCR 和单核 RNAseq，我们发现 CB2 在所有研究的脑区都有低水平表达，主要是由少数小胶质细胞表达，神经元的表达比例更低。在脂多糖刺激（模拟非无菌条件下的神经炎症）下，我们证明炎症反应与脑组织中，尤其是小胶质细胞中的 CB2 mRNA 水平短暂降低有关。这一结果在 BV2 小胶质细胞系中得到了证实，它与在干扰素-γ 刺激下观察到的 CB2 mRNA 水平和炎症反应之间的正相关性形成了鲜明对比，后者模拟了无菌条件下的神经炎症。因此，大脑中 CB2 的表达可能会根据炎症环境的不同而上调或下调。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Journal of Neuroinflammation 医学-神经科学

CiteScore

15.90

自引率

3.20%

发文量

276

审稿时长

1 months

期刊介绍： The Journal of Neuroinflammation is a peer-reviewed, open access publication that emphasizes the interaction between the immune system, particularly the innate immune system, and the nervous system. It covers various aspects, including the involvement of CNS immune mediators like microglia and astrocytes, the cytokines and chemokines they produce, and the influence of peripheral neuro-immune interactions, T cells, monocytes, complement proteins, acute phase proteins, oxidative injury, and related molecular processes. Neuroinflammation is a rapidly expanding field that has significantly enhanced our knowledge of chronic neurological diseases. It attracts researchers from diverse disciplines such as pathology, biochemistry, molecular biology, genetics, clinical medicine, and epidemiology. Substantial contributions to this field have been made through studies involving populations, patients, postmortem tissues, animal models, and in vitro systems. The Journal of Neuroinflammation consolidates research that centers around common pathogenic processes. It serves as a platform for integrative reviews and commentaries in this field.