EZH2 Promotes Extracellular Matrix Degradation via Nuclear Factor-κB (NF-κB) and p38 Signaling Pathways in Pulpitis

Pulpitis is a complicated chronic inflammatory process which can be in a dynamic balance between damage and repair. The extracellular matrix plays an important regulatory role in wound healing and tissue repair. The aim of this study was to explore the role of the epigenetic mark, enhancer of zeste homolog 2 (EZH2) on the degradation of extracellular matrix during pulpitis. Quantitative polymerase chain reaction was used to assess the expression of matrix metalloproteinases (MMPs) and type I collagen in human dental pulp cells (HDPCs) upon EZH2 and EI1 (EZH2 inhibitor) stimulation. The mechanism of EZH2 affecting extracellular matrix was explored through quantitative polymerase chain reaction and Western blot. A rat model of dental pulp inflammation was established, and the expression of type I collagen in dental pulp under EZH2 stimulation was detected by immunohistochemical staining. EZH2 upregulated the expression of MMP-1, MMP-3, MMP-8, and MMP-10 and decreased the production of type I collagen in HDPCs, while EI1 had the opposite effect. EZH2 activated the nuclear factor-kappa B (NF-kappa B) and p38 signaling pathways in HDPCs, the inhibition of which reversed the induction of MMPs and the suppression of type I collagen. EZH2 can downregulate the type I collagen levels in an experimental model of dental pulpitis in rats. EZH2 promotes extracellular matrix degradation via nuclear factor-kappa B (NF-kappa B) and P38 signaling pathways in pulpitis. EZH2 can decrease the type I collagen levels in vivo and in vitro.