Identification and Verification of Hub mRNA-miRNA-lncRNA Network on Psoriasis by Integrated Bioinformatics Analysis
Identification and Verification of Hub mRNA-miRNA-lncRNA Network on Psoriasis by Integrated Bioinformatics Analysis
Wen-Da Wang1, Wei-Yue Gong1, Bin Li2, Shan-Shan Lei3* and Qing-Hua Wang1*
ABSTRACT
Psoriasis is an immune-mediated skin disease with a high incidence, it has been demonstrated that particular long non-coding RNAs (lncRNAs) are vital in psoriasis. However, their exact functions and regulatory mechanisms in psoriasis remain unclear. In this study, GSE142582 and GSE54456 datasets from GEO database were used to screen differentially expressed microRNAs (DEmiRNAs) and mRNAs (DEmRNAs) between psoriatic lesions and normal skin. Gene ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway, and protein-protein interaction (PPI) network analysis were performed to determine the enrichment pathway and hub mRNA targets. miRWalk database was used to predict the corresponding mRNA to DEmiRNAs, and StarBase database was utilized to predict LncRNA to DEmiRNAs. Hub lncRNA-miRNA-mRNA networks were integrated and constructed, and visualized using Cytoscape software. A psoriasis rat model was subsequently established to verify the hub lncRNA-miRNA-mRNA networks in psoriasis using RT-qPCR. The results demonstrated that, 813 DEmRNAs and 299 DEmiRNAs were identified. GO and KEGG analyses showed that up-regulated DEmRNAs were enriched for immune responses, inflammatory responses, and keratinization, while down-regulated DEmRNAs were enriched for intermediate filament organization and tight junctions. RT-qPCR analysis showed that the expression of lncRNA NEAT1, miR-135b-5p were significantly increased (p <0.05) compared to the normal group, while the levels of lncRNA MALAT1, lncRNA XIST, miR-125b-5p, miR-125b-2-3p, KIF2C, MYLK, ACTG2 and MYH11 were significantly decreased (p <0.01 and 0.05). In conclusion, the present study suggested that, over-activated immune and inflammatory systems, hyperkeratosis, and cell junction destruction were the main biological reactions driving the development of psoriasis. The lncRNA (NEAT1)-miRNA (miR-125b-5p, miR-125b-2-3p)-mRNA (KIF2C) axis, and lncRNA (MALAT1, XIST)-miRNA (miR-135b-5p)-mRNA (MYLK, ACTG2, and MYH11) axis play vital roles in the pathogenesis of psoriasis, which may be the important mechanisms to explain the happen and progression of psoriasis.
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