Abstract
The etiology of schizophrenia (SCZ), as a serious mental illness, is unknown. The significance of genetics in SCZ pathophysiology is yet unknown, and newly identified mechanisms involved in the regulation of gene transcription may be helpful in determining how these changes affect SCZ development and progression. In the current work, we used a bioinformatics approach to describe the role of long non-coding RNA (lncRNA)-associated competing endogenous RNAs (ceRNAs) in the olfactory epithelium (OE) samples in order to better understand the molecular regulatory processes implicated in SCZ disorders in living individuals. The Gene Expression Omnibus database was used to obtain the OE microarray dataset (GSE73129) from SCZ sufferers and control subjects, which contained information about both lncRNAs and mRNAs. The limma package of R software was used to identify the differentially expressed lncRNAs (DElncRNAs) and mRNAs (DEmRNAs). RNA interaction pairs were discovered using the Human MicroRNA Disease Database, DIANA-LncBase, and miRTarBase databases. In this study, the Pearson correlation coefficient was utilized to find positive correlations between DEmRNAs and DElncRNAs in the ceRNA network. Eventually, lncRNA-associated ceRNA axes were developed based on co-expression relations and DElncRNA-miRNA-DEmRNA interactions. This work found six potential DElncRNA-miRNA-DEmRNA loops in SCZ pathogenesis, including, SNTG2-AS1/hsa-miR-7-5p/SLC7A5, FLG-AS1/hsa-miR-34a-5p/FOSL1, LINC00960/hsa-miR-34a-5p/FOSL1, AQP4-AS1/hsa-miR-335-5p/FMN2, SOX2-OT/hsa-miR-24-3p/NOS3, and CASC2/hsa-miR-24-3p/NOS3. According to the findings, ceRNAs in OE might be promising research targets for studying SCZ molecular mechanisms. This could be a great opportunity to examine different aspects of neurodevelopment that may have been hampered early in SCZ patients.
Highlights
A century after an influential work done by Kraepelin on the subject of dementia praecox, schizophrenia spectrum disorder (SSD) is still mysterious in terms of its different etiologies, symptomatology, the unpredictability of disease progression, moderate therapeutic outcomes, and the concern of comorbidities like obesity, diabetes, and tobacco use d isorder[1,2,3]
Aberrant gene expression and protein production are associated with SCZ pathophysiology, and these alterations in SCZ patients occur in multiple brain regions and have temporal variation during disease p rogression[7,8,9]
Background adjustment, normalization, gene filtering, and batch adjustment were done before performing Differential expression gene analysis (DEGA)
Summary
A century after an influential work done by Kraepelin on the subject of dementia praecox, schizophrenia spectrum disorder (SSD) is still mysterious in terms of its different etiologies, symptomatology, the unpredictability of disease progression, moderate therapeutic outcomes, and the concern of comorbidities like obesity, diabetes, and tobacco use d isorder[1,2,3]. A growing body of evidence has indicated alterations in non-coding RNAs (ncRNAs) in SCZ p atients[10] These findings help elucidate the molecular mechanisms underlying the dysregulation of gene expression and protein production. Accumulating evidence has revealed the aberrant expression of microRNAs (miRNAs) (20–22 nucleotides)[12,13] and long non-coding RNAs (lncRNAs), with over 200 nucleotides, in the brain of SCZ patients, which implicates in the occurrence and development of SCZ14,15. The recently identified molecular mechanisms regulating gene transcription could help elucidate how the alterations in gene expression could affect SCZ development and progression. We performed a bioinformatics analysis to identify lncRNA-associated ceRNA axes in the OE of live SCZ patients to elucidate molecular regulatory mechanisms related to the disease
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