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探索重度抑郁症中男性特异性突触可塑性:使用生物信息学方法的单核转录组分析

Exploring Male-Specific Synaptic Plasticity in Major Depressive Disorder: A Single-Nucleus Transcriptomic Analysis Using Bioinformatics Methods.

作者信息

Chen Ji, Zhu Xiumei, Yang Fan, Liu Yanan, Ba Huajie, Huang Ping, Wang Hongyan, Bian Yingnan, Li Chengtao, Zhang Suhua

机构信息

Institute of Forensic Science, Fudan University, Shanghai 200032, China.

School of Forensic Medicine, China Medical University, Shenyang 110122, China.

出版信息

Int J Mol Sci. 2025 Mar 28;26(7):3135. doi: 10.3390/ijms26073135.

DOI:10.3390/ijms26073135
PMID:40243907
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11989135/
Abstract

Major depressive disorder (MDD) is a complex psychiatric illness, with synaptic plasticity playing a key role in its pathology. Our study aims to investigate the molecular basis of MDD by analyzing synaptic plasticity-related gene expression at the single-cell level. Utilizing a published snRNA-seq dataset (GSE144136), we identified Excitatory.neurons_1 as the cell cluster most associated with MDD and synaptic plasticity through cell clustering, gene set enrichment analysis (GSEA), and pseudotime analysis. Integrating the bulk RNA-seq data (GSE38206), we identified CASKIN1 and CSTB as hub genes via differential expression analysis and machine learning methods. Further exploration of the relevant mechanisms was performed via cell-cell communication and ligand-receptor interaction analysis, functional enrichment analysis, and the construction of molecular regulatory networks, highlighting miR-21-5p as a key biomarker. We propose that elevated miR-21-5p in MDD downregulates CASKIN1 in Excitatory.neurons_1 cells, resulting in decreased neural connectivity and altered synaptic plasticity. As our analyzed snRNA-seq dataset consists solely of male samples, these findings may be male-specific. Our findings shed light on potential mechanisms underlying synaptic plasticity in MDD, offering novel insights into the disorder's cellular and molecular dynamics.

摘要

重度抑郁症(MDD)是一种复杂的精神疾病,突触可塑性在其病理过程中起关键作用。我们的研究旨在通过在单细胞水平分析与突触可塑性相关的基因表达来探究MDD的分子基础。利用已发表的单细胞核RNA测序数据集(GSE144136),我们通过细胞聚类、基因集富集分析(GSEA)和拟时间分析,将兴奋性神经元1鉴定为与MDD和突触可塑性最相关的细胞簇。整合批量RNA测序数据(GSE38206),我们通过差异表达分析和机器学习方法将CASKIN1和CSTB鉴定为核心基因。通过细胞间通讯和配体-受体相互作用分析、功能富集分析以及分子调控网络的构建,对相关机制进行了进一步探索,突出了miR-21-5p作为关键生物标志物。我们提出,MDD中miR-21-5p的升高会下调兴奋性神经元1细胞中的CASKIN1,导致神经连接性降低和突触可塑性改变。由于我们分析的单细胞核RNA测序数据集仅包含男性样本,这些发现可能具有男性特异性。我们的研究结果揭示了MDD中突触可塑性的潜在机制,为该疾病的细胞和分子动力学提供了新的见解。

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本文引用的文献

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Single-cell RNA-seq reveals the role of YAP1 in prefrontal cortex microglia in depression.单细胞 RNA 测序揭示了 YAP1 在抑郁症前额叶皮层小胶质细胞中的作用。
BMC Neurol. 2024 Jun 7;24(1):191. doi: 10.1186/s12883-024-03685-1.
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Single-nucleus transcriptomic analysis reveals the relationship between gene expression in oligodendrocyte lineage and major depressive disorder.单核转录组分析揭示了少突胶质细胞谱系中的基因表达与重度抑郁症之间的关系。
J Transl Med. 2024 Jan 27;22(1):109. doi: 10.1186/s12967-023-04727-x.
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Pathological Deficit of Cystatin B Impairs Synaptic Plasticity in EPM1 Human Cerebral Organoids.
胱抑素 B 的病理性缺失损害 EPM1 人神经脑类器官中的突触可塑性。
Mol Neurobiol. 2024 Jul;61(7):4318-4334. doi: 10.1007/s12035-023-03812-y. Epub 2023 Dec 12.
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Integrative Analyses of scRNA-seq, Bulk mRNA-seq, and DNA Methylation Profiling in Depressed Suicide Brain Tissues.抑郁自杀脑组织中单细胞 RNA-seq、 bulk mRNA-seq 和 DNA 甲基化谱的综合分析。
Int J Neuropsychopharmacol. 2023 Dec 18;26(12):840-855. doi: 10.1093/ijnp/pyad057.
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Cell type specific transcriptomic differences in depression show similar patterns between males and females but implicate distinct cell types and genes.抑郁中细胞类型特异性转录组差异在男性和女性中表现出相似的模式,但涉及不同的细胞类型和基因。
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Oxidative Stress in Depression: The Link with the Stress Response, Neuroinflammation, Serotonin, Neurogenesis and Synaptic Plasticity.抑郁症中的氧化应激:与应激反应、神经炎症、血清素、神经发生及突触可塑性的联系
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