Abstract
Purpose This study aimed to investigate the underlying molecular mechanisms of Parkinson's disease (PD) by bioinformatics. Methods Using the microarray dataset GSE72267 from the Gene Expression Omnibus database, which included 40 blood samples from PD patients and 19 matched controls, differentially expressed genes (DEGs) were identified after data preprocessing, followed by Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses. Protein-protein interaction (PPI) network, microRNA- (miRNA-) target regulatory network, and transcription factor- (TF-) target regulatory networks were constructed. Results Of 819 DEGs obtained, 359 were upregulated and 460 were downregulated. Two GO terms, “rRNA processing” and “cytoplasm,” and two KEGG pathways, “metabolic pathways” and “TNF signaling pathway,” played roles in PD development. Intercellular adhesion molecule 1 (ICAM1) was the hub node in the PPI network; hsa-miR-7-5p, hsa-miR-433-3p, and hsa-miR-133b participated in PD pathogenesis. Six TFs, including zinc finger and BTB domain-containing 7A, ovo-like transcriptional repressor 1, GATA-binding protein 3, transcription factor dp-1, SMAD family member 1, and quiescin sulfhydryl oxidase 1, were related to PD. Conclusions “rRNA processing,” “cytoplasm,” “metabolic pathways,” and “TNF signaling pathway” were key pathways involved in PD. ICAM1, hsa-miR-7-5p, hsa-miR-433-3p, hsa-miR-133b, and the abovementioned six TFs might play important roles in PD development.
Highlights
Parkinson’s disease (PD) is one of the most common agerelated neurodegenerative diseases [1]. e age at PD onset is approximately 55 years, and the incidence in the population aged > 65 years is approximately 1% [1,2,3]
Patients with PD present with symptoms such as bradykinesia, resting tremor, rigidity, and postural instability [5]. e current therapy for PD is targeted at its symptoms rather than at dopaminergic neuron degeneration [1]. e diagnosis of PD at the early stage is challenging, and successfully managing PD is difficult at its later stages [4]
Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses for the up- and downregulated differentially expressed genes (DEGs) were performed (Supplementary Table 2). e signi cant GO terms and KEGG pathways are shown in Figure 2. e upregulated DEGs were signi cantly enriched in four KEGG pathways, namely, metabolic pathways, inositol phosphate metabolism, mRNA surveillance pathway, and RNA degradation, and GO terms such as transcription, DNAtemplate processing, and ribosomal RNA (rRNA) processing (Figure 2(a))
Summary
Parkinson’s disease (PD) is one of the most common agerelated neurodegenerative diseases [1]. e age at PD onset is approximately 55 years, and the incidence in the population aged > 65 years is approximately 1% [1,2,3]. Much effort has been spent in investigating PD pathogenesis, and the misfolding, aggregation, and aberrance of proteins are considered to be some of the main causes [1, 4, 5]. Some key genes such as hydrogen sulfide, chromobox 5 (CBX5), and transcription factor 3 (TCF3) are related to PD [6, 7]. Activation of the protein kinase B (Akt)/glycogen synthase kinase 3 beta/(GSK3β) pathway by urate reportedly protects dopaminergic neurons in a rat model of PD [8].
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