MiR-155-5p modulates inflammatory phenotype of activated oral lichen-planus-associated-fibroblasts by targeting SOCS1

Abstract

Micro (MiR)-155-5p plays a vital role in inflammation and immune responses, but the function in oral lichen planus (OLP) remains unclear. Recent research has revealed that OLP associated-fibroblasts (OLP AFs) contribute to the inflammatory process with activated phenotype. This study was carried out to assess the role of miR-155-5p in the pro-inflammatory process of activated OLP AFs. Normal mucosal fibroblasts (NFs) and OLP AFs were isolated from oral mucosa of healthy controls and OLP patients respectively. We detected the expression of miR-155-5p and FAP-α in NFs and OLP AFs by real-time RT-PCR and calculated their correlation. Enzyme-linked immunosorbent assay was used to detect cytokine production. Immunohistochemistry and western blotting assay were used to detect suppressor of cytokine signaling 1 (SOCS1) expression. Dual-luciferase reporter assay was conducted to explore the interaction between miR-155-5p and SOCS1. MiR-155-5p and FAP-α were significantly increased in OLP AFs, and positively correlated. The expression of SOCS1 is decreased in the epithelial layer of OLP tissues and OLP AFs. Overexpression of miR-155-5p augmented interleukin-6 (IL-6) and interleukin-8 (IL-8) release. The knockdown of miR-155-5p in OLP AFs decreased IL-6 and IL-8 release. Furthermore, miR-155-5p inhibits SOCS1 expression by directly targeting its 3′-UTR in NFs and OLP AFs. SOCS1 silencing augmented IL-6 and IL-8 production in NFs. Here, we suggest that miR-155-5p regulates the secretion of IL-6 and IL-8 by downregulating the expression of SOCS1 in activated OLP AFs. Our results provide novel insights into the pathogenesis of OLP and a new target for OLP future therapy.