miR‐205‐5p inhibits psoriasis‐associated proliferation and angiogenesis: Wnt/β‐catenin and mitogen‐activated protein kinase signaling pathway are involved

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.