背景:患有多囊卵巢综合征(PCOS)的女性并发抑郁的几率增加,表明PCOS与抑郁症之间的关系更可能是合并症。然而,潜在机制尚不清楚.这里,我们旨在利用生物信息学分析来筛选PCOS和抑郁症共有的遗传因素.
方法:使用NCBI中的PCOS和抑郁症数据集,通过GEO2R筛选出差异表达基因(DEGs)。进行蛋白质-蛋白质相互作用(PPI)网络分析和富集分析以鉴定潜在的hub基因。在使用其他PCOS和抑郁症数据集进行验证后,我们使用来自英国生物样本库(UKB)数据库的数据进一步研究了关键基因多态性与合并症之间的关联.
结果:在这项研究中,三个关键基因,即,SNAP23,VTI1A,和PRKAR1A,并在PCOS和抑郁症的共病中鉴定了它们在囊泡转运途径中的相关SNARE相互作用。SNAP23的rs112568544,PRKAR1A的rs11077579和rs4458066,VTI1A的rs10885349可能是这种共病的遗传基础。
结论:我们的研究表明,SNAP23,PRKAR1A,VTI1A基因可直接或间接参与PCOS与抑郁症共病的发病机制中SNAREs的不平衡组装。这些发现可能为这种共病的诊断和治疗提供新的策略。
Women with polycystic ovary syndrome (PCOS) have increased odds of concurrent depression, indicating that the relationship between PCOS and depression is more likely to be comorbid. However, the underlying mechanism remains unclear. Here, we aimed to use bioinformatic analysis to screen for the genetic elements shared between PCOS and depression.
Differentially expressed genes (DEGs) were screened out through GEO2R using the PCOS and depression datasets in NCBI. Protein-protein interaction (PPI) network analysis and enrichment analysis were performed to identify the potential hub genes. After verification using other PCOS and depression datasets, the associations between key gene polymorphism and comorbidity were further studied using data from the UK biobank (UKB) database.
In this study, three key genes, namely, SNAP23, VTI1A, and PRKAR1A, and their related SNARE interactions in the vesicular transport pathway were identified in the comorbidity of PCOS and depression. The rs112568544 at SNAP23, rs11077579 and rs4458066 at PRKAR1A, and rs10885349 at VTI1A might be the genetic basis of this comorbidity.
Our study suggests that the SNAP23, PRKAR1A, and VTI1A genes can directly or indirectly participate in the imbalanced assembly of SNAREs in the pathogenesis of the comorbidity of PCOS and depression. These findings may provide new strategies in diagnosis and therapy for this comorbidity.