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The aim of the present study was to establish an integrated network of DNA methylation and RNA expression in an ovalbumin (OVA)‑induced asthma model, and to investigate the epigenetically‑regulated genes involved in asthma development. Genome‑wide CpG‑DNA methylation profiling was conducted through the use of a methylated DNA immunoprecipitation microarray and RNA sequencing was performed using three lung samples from mice with OVA‑induced asthma. A total of 35,401 differentially methylated regions (DMRs) were identified between mice with OVA‑induced asthma and control mice. Of these, 3,060 were located in promoter regions and 370 of the genes containing these DMRs demonstrated an inverse correlation between methylation and gene expression. Kyoto Encyclopedia of Genes and Genomes pathway analysis identified that 368 genes were upregulated or downregulated in OVA‑induced asthma samples, including genes involved in 'chemokine signalling pathway', 'focal adhesion', 'leukocyte transendothelial migration' and 'vascular smooth muscle contraction signaling' pathways. Integrated network analysis identified four hub genes, consisting of three upregulated genes [forkhead box O1 (FOXO1), SP1 transcription factor (SP1) and amyloid β precursor protein (APP)], and one downregulated gene [RUNX family transcription factor 1 (RUNX1)], all of which demonstrated an association between DNA methylation and gene expression. These genes were highly interconnected nodes in the Ingenuity Pathway Analysis module and were functionally significant. A total of four interconnected hub genes, FOXO1, RUNX1, SP1 and APP, were identified from the integrated DNA methylation and gene expression networks involved in asthma development. These results suggested that modulating these four genes could effectively control the development of asthma.

Parkinson's disease (PD) is a progressive, degene-rative neurological disease, typically characterized by tremors and muscle rigidity. The present study aimed to identify differe-ntially expressed genes (DEGs) between patients with PD and healthy patients, and clarify their association with additional biological processes that may regulate factors that lead to PD. An integrated analysis of publicly available Gene Expression Omnibus datasets of PD was performed. DEGs were identified between PD and normal blood samples. Gene Ontology enrichment and Kyoto Encyclopedia of Genes and Genomes pathway analyses, as well as protein‑protein interaction (PPI) networks were used to predict the functions of identified DEGs. Reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR) was performed to validate the predicted expression levels of identified DEGs in whole blood samples obtained from patients with PD and normal healthy controls. A total of 292DEGs were identified between the PD and normal blood samples. Of these, 156 genes were significantly upregulated and 136 genes were significantly downregulated in PD samples following integrated analysis of four PD expression datasets. The 10 most upregulated and downregulated genes were used to construct a PPI network, where ubiquitin C‑terminal hydrolase L1 (UCHL1), 3‑phosphoinositide dependent protein kinase 1 (PDPK1) and protein kinase cAMP‑activated catalytic subunit β (PRKACB) demonstrated the highest connectivity in the network. DEGs were significantly enriched in amoebiasis, vascular smooth muscle contraction, and the Wnt and calcium signaling pathways. The expression levels of significant DEGs, UCHL1, PDPK1 and PRKACB were validated using RT‑qPCR analysis. The findings revealed that UCHL1 and PDPK1 were upregulated and PRKACB was downregulated in patients with PD when compared with normal healthy controls. In conclusion, the results indicate that the significant DEGs, including UCHL1, PDPK1 and PRKACB may be associated with the development of PD. In addition, these factors may be involved in various signaling pathways, including amoebiasis, vascular smooth muscle contraction and the Wnt and calcium signaling pathways.

Intracranial aneurysm (IA) is a cerebrovascular disease with a high mortality rate. The pathogenesis of IA remains unclear and the treatment limited. The purpose of the present study was to identify the key genes expressed in IAs and provide the basis for further research and treatment. The raw dataset GSE75436 was downloaded from Gene Expression Omnibus, including 15 IA samples and 15 matched superficial temporal artery (STA) samples. Then, differentially expressed genes (DEGs) were identified using the limma package in R software. Hierarchical clustering analysis was performed on the DEGs using the gplot2 package in R. Database for Annotation, Visualization, and Integrated Discovery (DAVID) online tools were used to perform gene ontology (GO) functional enrichment analysis. DAVID and gene set enrichment analysis were separately used to perform the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses. The intersections of the two results were selected as common KEGG pathways. Protein‑protein interaction (PPI) analysis among the DEGs involved in the common KEGG pathways was performed using Search Tool for the Retrieval of Interacting Genes online tools, and visualized with Cytoscape software. A total of 782 DEGs were identified, comprising 392 upregulated and 390 downregulated DEGs. Hierarchical clustering demonstrated that the DEGs could precisely distinguish the IAs from the STAs. The GO enrichment analysis demonstrated that the upregulated DEGs were mainly involved in the inflammatory response and the management of extracellular matrix, and the downregulated DEGs were mainly involved in the process of vascular smooth muscle contraction. The KEGG pathway enrichment analysis demonstrated that the common pathways were 'leishmaniasis', 'Toll‑like receptor signaling pathway' and 'vascular smooth muscle contraction'. In the PPI network, tumor necrosis factor (TNF), interleukin 8 and Toll‑like receptor 4 had the highest degrees; they were associated with the inflammatory response. The Toll‑like receptor signaling pathway and TNF gene may serve as targets for future research and treatment.