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脂肪量与肥胖介导的N6-甲基腺苷修饰调节创伤性脑损伤后的神经炎症反应。

Fat mass and obesity-mediated N 6 -methyladenosine modification modulates neuroinflammatory responses after traumatic brain injury.

作者信息

Chen Xiangrong, Lai Jinqing, Wu Zhe, Chen Jianlong, Yang Baoya, Chen Chunnuan, Ding Chenyu

机构信息

Department of Neurosurgery, Second Clinical Medical College, Second Affiliated Hospital of Fujian Medical University, Quanzhou, Fujian Province, China.

Department of Neurology, Second Clinical Medical College, Second Affiliated Hospital of Fujian Medical University, Quanzhou, Fujian Province, China.

出版信息

Neural Regen Res. 2026 Feb 1;21(2):730-741. doi: 10.4103/NRR.NRR-D-23-01854. Epub 2024 Sep 6.

DOI:10.4103/NRR.NRR-D-23-01854
PMID:39248160
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12220718/
Abstract

JOURNAL/nrgr/04.03/01300535-202602000-00042/figure1/v/2025-05-05T160104Z/r/image-tiff The neuroinflammatory response mediated by microglial activation plays an important role in the secondary nerve injury of traumatic brain injury. The post-transcriptional modification of N 6 -methyladenosine is ubiquitous in the immune response of the central nervous system. The fat mass and obesity-related protein catalyzes the demethylation of N 6 -methyladenosine modifications on mRNA and is widely expressed in various tissues, participating in the regulation of multiple diseases' biological processes. However, the role of fat mass and obesity in microglial activation and the subsequent neuroinflammatory response after traumatic brain injury is unclear. In this study, we found that the expression of fat mass and obesity was significantly down-regulated in both lipopolysaccharide-treated BV2 cells and a traumatic brain injury mouse model. After fat mass and obesity interference, BV2 cells exhibited a pro-inflammatory phenotype as shown by the increased proportion of CD11b + /CD86 + cells and the secretion of pro-inflammatory cytokines. Fat mass and obesity-mediated N 6 -methyladenosine demethylation accelerated the degradation of ADAM17 mRNA, while silencing of fat mass and obesity enhanced the stability of ADAM17 mRNA. Therefore, down-regulation of fat mass and obesity expression leads to the abnormally high expression of ADAM17 in microglia. These results indicate that the activation of microglia and neuroinflammatory response regulated by fat mass and obesity-related N 6 -methyladenosine modification plays an important role in the pro-inflammatory process of secondary injury following traumatic brain injury.

摘要

《期刊》/nrgr/04.03/01300535 - 202602000 - 00042/图1/v/2025 - 05 - 05T160104Z/图像 - tiff 小胶质细胞激活介导的神经炎症反应在创伤性脑损伤的继发性神经损伤中起重要作用。N6 - 甲基腺苷的转录后修饰在中枢神经系统的免疫反应中普遍存在。脂肪量与肥胖相关蛋白催化mRNA上N6 - 甲基腺苷修饰的去甲基化，在各种组织中广泛表达，参与多种疾病生物学过程的调节。然而，脂肪量与肥胖在创伤性脑损伤后小胶质细胞激活及随后的神经炎症反应中的作用尚不清楚。在本研究中，我们发现脂肪量与肥胖在脂多糖处理的BV2细胞和创伤性脑损伤小鼠模型中表达均显著下调。脂肪量与肥胖干扰后，BV2细胞表现出促炎表型，如CD11b + /CD86 + 细胞比例增加和促炎细胞因子分泌增加。脂肪量与肥胖介导的N6 - 甲基腺苷去甲基化加速了ADAM17 mRNA的降解，而脂肪量与肥胖的沉默增强了ADAM17 mRNA的稳定性。因此，脂肪量与肥胖表达下调导致小胶质细胞中ADAM17异常高表达。这些结果表明，脂肪量与肥胖相关的N6 - 甲基腺苷修饰调节的小胶质细胞激活和神经炎症反应在创伤性脑损伤后继发性损伤的促炎过程中起重要作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2825/12220718/13aef08db663/NRR-21-730-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2825/12220718/7a843fe7247f/NRR-21-730-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2825/12220718/6217301f73ca/NRR-21-730-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2825/12220718/c6aae6246190/NRR-21-730-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2825/12220718/0982bbbbc156/NRR-21-730-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2825/12220718/7fca36a7f83a/NRR-21-730-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2825/12220718/562d59ebe3d3/NRR-21-730-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2825/12220718/0aef20bd8551/NRR-21-730-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2825/12220718/13aef08db663/NRR-21-730-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2825/12220718/7a843fe7247f/NRR-21-730-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2825/12220718/6217301f73ca/NRR-21-730-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2825/12220718/c6aae6246190/NRR-21-730-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2825/12220718/0982bbbbc156/NRR-21-730-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2825/12220718/7fca36a7f83a/NRR-21-730-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2825/12220718/562d59ebe3d3/NRR-21-730-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2825/12220718/0aef20bd8551/NRR-21-730-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2825/12220718/13aef08db663/NRR-21-730-g009.jpg

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