Skin Pharmacology and Physiology
Wang Y. · Jiang F. · Chen F. · Zhang D. · Wang J.Log in to MyKarger to check if you already have access to this content.
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Article / Publication Details AbstractIntroduction: Psoriasis is an immune-mediated polygenic inflammatory skin disease, keratinocyte proliferation is an important mechanism. The study investigated the role and regulatory relationship between lncRNA XIST and miR-338-5p in psoriatic patients and cell models. Methods: Serum samples were collected from 55 psoriasis patients. HaCaT was recruited for the cell experiments, and induced by M5 cytokines to mimic psoriasis in vitro. XIST and miR-338-5p levels were detected via qRT-PCR. Cell viability under different treatments was evaluated using CCK-8. ELISA was applied to measure the concentration of inflammatory cytokines. The regulatory relationship was confirmed using luciferase reporter gene assay. Results: Serum XIST was elevated in patients with psoriasis, and can distinguish the psoriasis patients from healthy controls according to the ROC curve. High level of XIST was positively correlated with with PASI score and serum TNF-α, IL-17A and IL-22 concentrations in psoriasis patients. XIST silencing suppressed M5-induced keratinocyte proliferation and restrained the discharge of inflammatory cytokines (TNF-α, IL-17A, IL-22) and chemokines (CXCL1, CXCL8, CCL20). XIST can sponge miR-338-5p, and miR-338-5p downregulation abolished the inhibitory effect of XIST silencing on cell proliferation and inflammation. miR-338-5p was at high expression in the clinical serum samples from psoriasis patients. The target relationship between miR-338-5p and IL-6 was proved. Conclusion: LncRNA XIST is highly expressed in the serum of patients with psoriasis, and was positively correlated with disease severity and inflammation. XIST may regulate keratinocyte proliferation and inflammation via regulating miR-338-5p/IL-6 axis.
S. Karger AG, Basel
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