Wang Yanrong, Wang Yuan, Zhang Manxue, Liu Doudou, Fang Jianqun
Mental Health Centre, General Hospital of Ningxia Medical University, Ningxia, China.
Psychiatry Investig. 2024 May;21(5):464-474. doi: 10.30773/pi.2023.0149. Epub 2024 May 23.
We aimed to predict the possible mechanism of obsessive-compulsive disorder (OCD) by integrating and analyzing mRNA sequencing results from two datasets and to provide direction for future studies into the pathogenesis of OCD.
Two OCD datasets, GSE78104 and GSE60190, were obtained, and the intersection of the two gene sets with differential expression in OCD samples was selected. Kyoto Encyclopedia of Genes and Genomes (KEGG) signal pathway enrichment and Gene Ontology (GO) analyses were performed using the Database for Annotation, Visualization, and Integrated Discovery (DAVID) online analysis website for the genes at the intersection, and the data were mapped using http://www.bioinformatics.com.cn. After genes with p≤0.05 had been screened out, protein-protein interaction (PPI) interaction analysis was conducted using Metascape to screen the key Molecular Complex Detection (MCODE) genes. MCODE genes were then enriched using the KEGG signaling pathway and GO classification.
A total of 3,449 differentially expressed genes (DEGs) were obtained from the GSE78104 and GSE60190 datasets. KEGG, GO, and Gene Set Enrichment Analysis analyses of DEGs showed that the onset of OCD was related to oxidative phosphorylation and other metabolic processes, which may have a similar pathogenesis to other neurodegenerative diseases. Single-gene PPI analysis of SAPAP3 revealed that the mechanism by which SAPAP3 knockout induces OCD may also be caused by affecting oxidative phosphorylation.
The mechanism of SAPAP3 knockout-induced OCD in mice may be due to the oxidative phosphorylation process in the body. Future studies on the neural circuit mechanism of OCD should be conducted.
通过整合和分析两个数据集的mRNA测序结果，预测强迫症（OCD）的可能机制，为未来强迫症发病机制的研究提供方向。
获取两个强迫症数据集GSE78104和GSE60190，选择在强迫症样本中差异表达的两个基因集的交集。使用在线分析网站DAVID对交集中的基因进行京都基因与基因组百科全书（KEGG）信号通路富集和基因本体论（GO）分析，并使用http://www.bioinformatics.com.cn绘制数据。筛选出p≤0.05的基因后，使用Metascape进行蛋白质-蛋白质相互作用（PPI）相互作用分析，以筛选关键的分子复合物检测（MCODE）基因。然后使用KEGG信号通路和GO分类对MCODE基因进行富集。
从GSE78104和GSE60190数据集中共获得3449个差异表达基因（DEG）。对DEG的KEGG、GO和基因集富集分析表明，强迫症的发病与氧化磷酸化和其他代谢过程有关，这可能与其他神经退行性疾病有相似的发病机制。对SAPAP3的单基因PPI分析表明，SAPAP3基因敲除诱导强迫症的机制也可能是通过影响氧化磷酸化引起的。
小鼠中SAPAP3基因敲除诱导强迫症的机制可能是由于体内的氧化磷酸化过程。未来应开展关于强迫症神经回路机制的研究。
