Abstract
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-κB) 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-κB (NF-κB) and P38 signaling pathways in pulpitis. EZH2 can decrease the type I collagen levels in vivo and in vitro.
Highlights
Dental pulp is derived from ectodermal stroma and is a loose connective tissue rich in extracellular matrix (ECM)
Results :enhancer of zeste homolog 2 (EZH2) upregulated the expression of matrix metalloproteinases (MMPs)-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-kB(NF-kB)and p38 signaling Pathways in HDPCs, the inhibition of which reversed the induction of MMPs and the suppression of type I collagen .EZH2 can downregulated the type I collagen levels in an experimental model of dental pulpitis in rats
We addressed the following hypothesis: EZH2 affects the expression of MMP in dental pulp through the nuclear factor kappa B (NF-kB) pathway or Mitogen-activated Protein Kinase (MAPK) pathway, thereby mediating the degradation of extracellular matrix and affecting the progress of dental pulp inflammation such as the collagen degradation
Summary
Dental pulp is derived from ectodermal stroma and is a loose connective tissue rich in extracellular matrix (ECM). HDPCs, the main dental pulp component, can interact with immune cells to secrete significant amounts of inflammatory cytokines and chemokines locally. These cytokines and chemokines may promote pulpitis progression, tissue destruction, or regulate inflammatory responses to eliminate pathogens[3, 4]. Recent studies have proved that ECM plays an important regulatory role in cell proliferation, differentiation, wound healing and tissue repair[5]. Extracellular matrix plays an important regulatory role in wound healing and tissue repair. The aim of this study was to explore role of the epigenetic mark, enhancer of zeste homolog 2 (EZH2) on the degradation of extracellular matrix during pulpitis
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