Chen Ji, Zhu Xiumei, Yang Fan, Liu Yanan, Ba Huajie, Huang Ping, Wang Hongyan, Bian Yingnan, Li Chengtao, Zhang Suhua
Institute of Forensic Science, Fudan University, Shanghai 200032, China.
School of Forensic Medicine, China Medical University, Shenyang 110122, China.
Int J Mol Sci. 2025 Mar 28;26(7):3135. doi: 10.3390/ijms26073135.
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.
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。