Abstract
Psoriasis is a chronic inflammatory skin disease, and the mechanism remains unknown. The present study found that the level of miR-205-5p was downregulated in psoriatic skin tissues. miR-205-5p inhibited proliferation in HaCaT cells. miR-205-5p impaired proliferation, migration and tube formation in human umbilical vein endothelial cells. Angiopoietin (Ang)-2, vascular endothelial growth factor (VEGFA) and bone morphogenetic protein and activin membrane-bound inhibitor (BAMBI) were confirmed as the targets of miR-205-5p. Moreover, miR-205-5p suppressed the phosphorylation of p38 and extracellular regulated protein kinase, and inhibited expression level of β-catenin. In vivo, miR-205-5p significantly alleviated imiquimod (IMQ)-induced psoriasis in mice, and deactivated mitogen-activated protein kinase (MAPK) and Wnt/β-catenin pathways. In summary, we demonstrated that miR-205-5p alleviated IMQ-induced psoriasis in mice by restraining epidermal hyperproliferation and excessive neovascularization. miR-205-5p may play its roles by targeting Ang-2, VEGFA and BAMBI, and deactivating the Wnt/β-catenin and MAPK signaling pathways. These findings may provide a potential therapeutic target for clinical treatment of psoriasis.