Abstract
The study aimed to screen potential key genes related to childhood atopic asthma based on an integrated analysis of gene expression and methylation profiles, as well as provide potential therapeutic targets for the progression of childhood atopic asthma. The gene expression profile of nasal epithelial cells GSE65204 (including 36 atopic asthma patients and 33 healthy controls) and the corresponding methylation profile GSE65163 (including 36 atopic asthma and 36 healthy controls) were obtained from the Gene Expression Omnibus. Following differentially expressed genes (DEGs) and differentially methylated positions (DMPs) were identified, correction analysis between DEGs and DMPs was conducted. Function and pathway-enrichment analyses were also performed for these candidate genes. Protein–protein interaction (PPI) and transcription factor (TF) regulatory networks were constructed. A total of 199 methylated DEGs were selected in childhood atopic asthma samples. Most were highly correlated with functions in the inflammatory response and the T cell receptor (TCR) signaling pathway. Moreover, CD8A, FYN, LCK, CXCR6, CCL5, and POSTN with differentially methylated sites in their promoter regions were significantly negatively correlated with their gene expression levels, and were found to have high degrees in the PPI network. In addition, TF MAZ may play an important role in the development of childhood atopic asthma by binding its targets, such as CD8A, FYN, and LCK. The methylated genes, CD8A, FYN, LCK, CXCR6, CCL5, and POSTN, may be closely associated with the pathogenesis of childhood atopic asthma owing to their roles in the inflammatory response and in the TCR signaling pathway.
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