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Published on: January 7, 2019
The identification of potentially key genes in cell aging and bronchial asthma by integrated bioinformatics analysis
Lingyu Pan1, Yeke Jiang2, Dezhi Yuan3
1The First Affiliated Hospital of Anhui University of Chinese Medicine, Hefei, 230031, Anhui, China; Anhui Hospital of Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Hefei, 230031, Anhui, China.
Background:
As cell aging is closely related to the onset of bronchial asthma (BA), discovering new potential targets for BA treatment from the perspective of cell senescence is important.
Methods:
BA-associated gene expression data.sets (GSE143303 and GSE147878) were downloaded from the Gene Expression Omnibus (GEO) database and screened for differential expression gene (DEG) and functional enrichment analyses. Weighted gene co-expression network analysis (WGCNA) was used to identify differential genes. Human Aging Genomic Resources, Aging Atlas, and MSigDB gene sets were used to collect genes related to cell aging. Age-related genes and key modules were combined to obtain intersection genes, which were analyzed for protein-protein interaction. The expression levels of cell aging DEG were analyzed in the GSE143303, followed by plotting receiver operating characteristic (ROC) curves and validating key differential genes in the GSE147878. The GSEA was used to analyze hub genes. Finally, Western blotting was used to detect the expression levels of cell aging markers and hub genes.
Results:
A total of 580 comprehensive DEGs were obtained from the GSE143303. CBX6, EP300, NFE2L2, and KMT2A were identified as central genes. Western blot showed that the levels of p16 and p21 were significantly increased in the BA model group, indicating that there was cell aging in BA rats, with Kechuanping granule (KCP) having a regulatory effect. CBX6, EP300, NFE2L2, and KMT2A expressions were changed in BA rats, and KCP had a regulatory effect on hub genes.
Conclusions:
The improvement of asthma by KCP may be closely related to the regulation of ASMCs aging by CBX6, EP300, NFE2L2, and KMT2A.
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