The mechanism of IL‐13 targeting IL‐13Rα2 in regulating oral mucosal FBs through PI3K/AKT/mTOR

Abstract

AbstractObjectiveThe objective of this investigation was to examine the presence of interleukin (IL)‐13 and its receptor IL‐13Rα2 in the tissues of oral submucous fibrosis (OSF), investigate their biological functions, and explore the underlying mechanisms involved in the development of OSF.Materials and MethodsThe expression of IL‐13 and IL‐13Rα2 in the oral mucosa of patients with OSF and normal individuals was determined through immunohistochemistry and reverse transcription–quantitative polymerase chain reaction (RT–qPCR). Primary fibroblasts (FBs) were extracted through enzymatic digestion and then cultured. Immunofluorescence was employed to identify the FB cultures and the location of IL‐13Rα2. The effects of IL‐13/IL‐13Rα2/PI3K/AKT/mTOR on the migration, proliferation, and secretion of fiber‐related proteins of FBs were explored via the wound healing assay, CCK‐8 assay, EDU assay, and RT–qPCR. The impact of IL‐13Rα2 silencing and PI3K/AKT inhibition on the effect of IL‐13 on FBs was analyzed by RT–qPCR and Western blotting.ResultsIL‐13 and IL‐13Rα2 were highly expressed in OSF. Primary FBs were successfully extracted and cultured. IL‐13Rα2 was found to be localized in myofibroblasts. IL‐13 promoted the proliferation, migration, and secretion of fibril‐associated proteins in FBs. The proliferation, migration, and secretion of fibril‐associated proteins of FBs were decreased following IL‐13Rα2 silencing and inhibition of the PI3K/AKT/mTOR pathway.ConclusionIL‐13 may promote the proliferation, migration, and secretion of fiber‐related proteins of FBs through the PI3K/AKT/mTOR pathway by targeting IL‐13Rα2.