Objective: To study the expression of Fra2, a member of Fos family of transcription factor AP1 family, in peripheral blood mononuclear cells (PBMC) of psoriatic patients, and to analyze the potential genes regulated by Fra2 via bioinformatics and confirmed by dual-luciferase reporter assay for investigating the role of Fra2 in the pathogenesis of psoriasis. Methods: The expression of Fra2 in 21 patients with psoriasis and 30 healthy controls were detected by quantitative real-time-PCR（qrt-RCR）. The target genes of Fra2 were predicted by gene transcription regulation Database (GTRD), and were intersected with psoriasis-related gene in GeneCards. The function classification of Gene Ontology (GO)and KEGG enrichment analysis were adopted by DAVID (The Database for Annotation, Visualization and Integrated Discovery); the potential genes regulated by Fra2 were verified by qrt -PCR; the binding sites of Fra2 were predicted by JASPAR package in R Programming Language;the relationship between Fra2 and IL23 receptor(IL23R) was verified by Dual-luciferase report assay. Results: The expression of Fra2 mRNA in PBMC of 21 patients with psoriasis (0.711±0.072) was significantly lower than that in healthy controls (1.070±0.086) (P=0.004 2). Bioinformatics analysis showed that inflammatory response and cytokine-cytokine receptor interaction was the most significant items(P=5.2×10-71; P=7.0×10-45). qrt-PCR found that the mRNA expression level of IL23R was significantly higher than healthy controls (P=0.000 1), and was correlated with Fra2 expression level(r=-0.509 5, P=0.018 3); the regulating effect of Fra2 on IL23R was verified by Dual-luciferase report assay. Conclusions: Fra2 is an important transcription factor involved in the development and progress of psoriasis by regulating the expression of IL23R.
LIN Zhen, GUO Ruru, LÜ Liangjing, CHEN Xiaoxiang
. Study on the involving of Fra2 via regulating IL23 receptor in the pathogenesis of psoriasis[J]. Journal of Diagnostics Concepts & Practice, 2018
, 17(03)
: 254
-259
.
DOI: 10.16150/j.1671-2870.2018.03.005
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