miR-203 contributes to IL-17-induced VEGF secretion by targeting SOCS3 in keratinocytes

Abstract

Interleukin (IL)-17 signaling serves an important role in the development and pathogenesis of psoriasis; a chronic skin disease characterized by increased dermal vascularity and the hyperproliferation of keratinocytes. microRNA (miR)-203 is preferentially expressed in the skin and is an important regulator of keratinocyte differentiation. miR-203 has been implicated in a number of skin diseases, including psoriasis. However, the role of miR-203 in IL-17-induced vascular endothelial growth factor (VEGF) secretion has yet to be elucidated. The present study demonstrated that miR-203 expression was upregulated in the ears of IL-17-stimulated mice and IL-17-treated HaCaT cells. In addition, the IL-17-induced increase in miR-203 expression activated the Janus kinase/signal transducer and activator of transcription signaling pathway and promoted VEGF secretion in HaCaT cells. Furthermore, miR-203 was observed to bind to the 3'-untranslated region of suppressor of cytokine signaling 3 (SOCS3) and inhibited SOCS3 expression. The results suggest that miR-203 expression may be upregulated by IL-17 stimulation, and miR-203 is a positive regulator of IL-17-induced VEGF secretion. The present study may support potential therapeutic strategies for the treatment of psoriasis.