Suppr超能文献

背根神经节-坐骨神经神经网络推断的外周感觉神经元细胞衰老及衰老表型的全基因组网络分析

Genome-Wide Network Analysis of DRG-Sciatic Nerve Network-Inferred Cellular Senescence and Senescence Phenotype in Peripheral Sensory Neurons.

作者信息

Kawabata Sora, Iijima Hirotaka, Kanemura Naohiko, Murata Kenji

机构信息

Department of Health and Social Services, Health and Social Services, Graduate School of Saitama Prefectural University, Saitama, Japan.

Japan Society for the Promotion of Science, Tokyo, Japan.

出版信息

Mol Neurobiol. 2025 May;62(5):6112-6127. doi: 10.1007/s12035-024-04666-8. Epub 2024 Dec 23.

Abstract

Accumulation of senescent neurons in the dorsal root ganglion (DRG) is an important tissue phenotype that causes age-related degeneration of peripheral sensory nerves. Senescent neurons are neurons with arrested cell cycle that have undergone cellular senescence but remain in the tissue and play various biological roles. To understand the accumulation of senescent neurons in the DRG during aging, we aimed to elucidate the mechanism that induces cellular senescence in DRG neurons and the role of senescent DRG neurons. We integrated multiple public transcriptome datasets for DRGs, which include cell bodies in neurons, and the sciatic nerve, which includes axons in neurons, using network medicine-based bioinformatics analysis. We thus inferred the molecular mechanisms involved in cellular senescence of DRG neurons, from molecular responses to senescence, in the DRG-sciatic nerve network. Network medicine-based bioinformatics analysis revealed that age-related Mapk3 decline leads to impaired cholesterol metabolism and biosynthetic function in axons, resulting in compensatory upregulation of Srebf1, a transcription factor involved in lipid and cholesterol metabolism. This in turn leads to CDKN2A-mediated cellular senescence. Furthermore, our analysis revealed that senescent DRG neurons develop a senescence phenotype characterized by activation of antigen-presenting cells via upregulation of Ctss as a hub gene. B cells were inferred as antigen-presenting cells activated by Ctss, and CD8-positive T cells were inferred as cells that receive antigen presentation from B cells.

摘要

背根神经节(DRG)中衰老神经元的积累是导致外周感觉神经发生与年龄相关退变的一种重要组织表型。衰老神经元是细胞周期停滞的神经元,它们已经经历了细胞衰老,但仍留在组织中并发挥各种生物学作用。为了了解衰老过程中DRG中衰老神经元的积累情况,我们旨在阐明诱导DRG神经元细胞衰老的机制以及衰老DRG神经元的作用。我们使用基于网络医学的生物信息学分析,整合了多个关于DRG的公共转录组数据集(其中包括神经元的细胞体)和坐骨神经的公共转录组数据集(其中包括神经元的轴突)。因此,我们从DRG - 坐骨神经网络中对衰老的分子反应推断出DRG神经元细胞衰老所涉及的分子机制。基于网络医学的生物信息学分析表明,与年龄相关的Mapk3下降导致轴突中胆固醇代谢和生物合成功能受损,从而导致参与脂质和胆固醇代谢的转录因子Srebf1的代偿性上调。这进而导致CDKN2A介导的细胞衰老。此外,我们的分析表明,衰老的DRG神经元通过上调作为枢纽基因的Ctss形成一种以抗原呈递细胞激活为特征的衰老表型。B细胞被推断为被Ctss激活的抗原呈递细胞,而CD8阳性T细胞被推断为接受B细胞抗原呈递的细胞。

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