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Identification of Molecular Signatures in Mild Intrinsic Atopic Dermatitis by Bioinformatics Analysis. | LitMetric

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Article Abstract

Background: Atopic dermatitis (AD) is recognized as a common inflammatory skin disease and frequently occurred in Asian and Black individuals.

Objective: Since the limitation of dataset associated with human severe AD, this study aimed to screen potential novel biomarkers involved in mild AD.

Methods: Expression profile data (GSE75890) were obtained from the database of Gene Expression Omnibus. Using limma package, the differentially expressed genes (DEGs) between samples from AD and healthy control were selected. Furthermore, function analysis was conducted. Meanwhile, the protein-protein interaction (PPI) network and transcription factor (TF)-miRNA-target regulatory network were constructed. And quantitative real-time polymerase chain reaction (qRT-PCR) was used to validate the expressions patterns of key genes.

Results: In total, 285 DEGs including 214 upregulated and 71 downregulated genes were identified between samples from two groups. The upregulated DEGs were mainly involved in nine pathways, such as hematopoietic cell lineage, pertussis, p53 signaling pathway, staphylococcus aureus infection, and cell cycle, while tight junction was the only pathway enriched by the downregulated DEGs. Cyclin B (CCNB)1, CCNB2, cyclin A (CCNA)2, C-X-C motif chemokine ligand (CXCL)10, and CXCL9 were key nodes in PPI network. The TF-miRNA-target gene regulatory network focused on miRNAs such as miR-106b, miR-106a, and miR-17, TFs such as nuclear factor kappa B subunit 1, RELA proto-oncogene, Sp1 transcription factor, and genes such as matrix metallopeptidase 9, peroxisome proliferator activated receptor gamma , and serpin family E member 1. Moreover, the upregulation of these genes, including , , , , and were confirmed by qRT-PCR.

Conclusion: , , , and might be novel markers of mild AD. miR-106b and miR-17 may involve in regulation of immune response in AD patients.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7992548PMC
http://dx.doi.org/10.5021/ad.2020.32.2.130DOI Listing

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