ASH1L Suppresses Matrix Metalloproteinase through Mitogen-activated Protein Kinase Signaling Pathway in Pulpitis

Yin, Bo; Hui, Tianqian; Yu, Fanyuan; Luo, Haiyong; Liao, Xueyang; Yang, Jing; Wang, Chenglin; Ye, Ling

doi:10.1016/j.joen.2016.10.020

Cited by 15 publications

(19 citation statements)

References 39 publications

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“…3). These results are in accordance with previous studies showing that ASH1L (absent, small, or homeotic 1-like, an H3K4 methyltransferase that can antagonize EZH2) signi cantly upregulate the expression of MMP-1, MMP-2 and MMP-13 through the Mitogen-activated Protein Kinase (MAPK) signaling pathway [16].In the rat experimental pulp infection model, EZH2 decreased the expression of Col-1, but EI1 could not upregulate the expression of Col-1 in rat pulpitis. EI1 could increase the expression of Col-1 in vitro, suggesting that the development of pulpitis is a multifactor regulatory process, and inhibition of EZH2 alone is not enough to promote the repair of collagen bers.…”

Section: Discussionsupporting

confidence: 93%

“…To gain further insight into the mechanism underlying EZH2-induced cytokine/ chemokine expression in HDPCs, we examined the NF-kB and MAPK pathways, which have been suggested by previous reports to be involved in modulating cytokine/chemokine expression [15,16].EZH2 treatment led to the activation of the MAPK and NF-kB pathways, as demonstrated by phosphorylation of those signaling molecules after 15-45 min of stimulation (Fig.3A).When we treated the HDPC with NF-kB inhibitor (BAY11-7082) or speci c p38(SB203580) inhibitor, the expression of phosphorylation of those signaling molecules were decreased( Fig.3B-C). The EZH2 -mediated induction of MMP-1 MMP-3 MMP-8 and MMP-10 expression decreased signi cantly by treatment with an NF-kB inhibitor (BAY11-7082) or p38(SB203580) inhibitors in 2 hours ( Fig.…”

Section: Ezh2 Promotes Ecm Degradation Via Nf-kb and P38 Signaling Pamentioning

confidence: 99%

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EZH2 Promotes Extracellular Matrix Degradation via Nuclear Factor-kB(NF-kB)and p38 signaling Pathways in Pulpitis.

Qin

Chen

et al. 2020

Preprint

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Background: Pulpitis is a complicated chronic inflammatory process which in a dynamic balance between damage and repair. 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. Methods : Quantitative polymerase chain reaction was used to assess the expression of matrix metalloproteinases (MMPs) and type I collagen in HDPCs upon EZH2 and EI1 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. Results :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-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. Conclusion: EZH2 promotes extracellular matrix degradation via Nuclear Factor-kB(NF-kB)and P38 signaling pathways in pulpitis.EZH2 can decrease the type I collagen levels in vivo and vitro.

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Section: Discussionsupporting

confidence: 93%

Section: Ezh2 Promotes Ecm Degradation Via Nf-kb and P38 Signaling Pamentioning

confidence: 99%

EZH2 Promotes Extracellular Matrix Degradation via Nuclear Factor-kB(NF-kB)and p38 signaling Pathways in Pulpitis.

Qin

Chen

et al. 2020

Preprint

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“…ASH1L is a mammalian homolog of Drosophila Ash, which activates the expression of multiple genes depending on the activity of the SET domain H3K4 methyltransferase [22,23]. The ASH1L gene is widely expressed in cells in vivo , including CD4 lymphocytes, macrophages, and natural killer (NK) cells [24,25]. Previously reported studies have shown that the expression of ASH1L inhibited interleukin-6 (IL-6) and toll-like receptor (TLR) that triggered the production of tumor necrosis factor (TNF) in a mouse model of sepsis [26].…”

Section: Discussionmentioning

confidence: 99%

Bioinformatics Analysis of Gene Expression Profiles for Risk Prediction in Patients with Septic Shock

Liu

Zhong

et al. 2019

Med Sci Monit

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BackgroundSeptic shock occurs when sepsis is associated with critically low blood pressure, and has a high mortality rate. This study aimed to undertake a bioinformatics analysis of gene expression profiles for risk prediction in septic shock.Material/MethodsTwo good quality datasets associated with septic shock were downloaded from the Gene Expression Omnibus (GEO) database, GSE64457 and GSE57065. Patients with septic shock had both sepsis and hypotension, and a normal control group was included. The differentially expressed genes (DEGs) were identified using OmicShare tools based on R. Functional enrichment of DEGs was analyzed using DAVID. The protein-protein interaction (PPI) network was established using STRING. Survival curves of key genes were constructed using GraphPad Prism version 7.0. Each putative central gene was analyzed by receiver operating characteristic (ROC) curves using MedCalc statistical software.ResultsGSE64457 and GSE57065 included 130 RNA samples derived from whole blood from 97 patients with septic shock and 33 healthy volunteers to obtain 975 DEGs, 455 of which were significantly down-regulated and 520 were significantly upregulated (P<0.05). Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis identified significantly enriched DEGs in four signaling pathways, MAPK, TNF, HIF-1, and insulin. Six genes, WDR82, ASH1L, NCOA1, TPR, SF1, and CREBBP in the center of the PPI network were associated with septic shock, according to survival curve and ROC analysis.ConclusionsBioinformatics analysis of gene expression profiles identified four signaling pathways and six genes, potentially representing molecular mechanisms for the occurrence, progression, and risk prediction in septic shock.

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“…To gain further insight into the mechanism underlying EZH2-induced cytokine/ chemokine expression in HDPCs, we examined the NF-κB and MAPK pathways, which have been suggested by previous reports to be involved in modulating cytokine/chemokine expression [15,16].EZH2 treatment led to the activation of the MAPK and NF-κB pathways, as demonstrated by phosphorylation of those signaling molecules after 15-45 min of stimulation (Fig.3A).When we treated the HDPC with NF-κB inhibitor (BAY11-7082) or speci c p38(SB203580) inhibitor, the expression of phosphorylation of those signaling molecules were decreased (Fig.3B-C). The EZH2 -mediated induction of MMP-1 MMP-3 MMP-8 and MMP-10 expression decreased signi cantly by treatment with an NF-κB inhibitor (BAY11-7082) or p38(SB203580) inhibitors in 2 hours (Fig.…”

Section: Ezh2 Promotes Ecm Degradation Via Nf-κb and P38 Signaling Pamentioning

confidence: 99%

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

Qin

Chen

et al. 2021

Preprint

View full text Add to dashboard Cite

Background: Pulpitis is a complicated chronic inflammatory process which in a dynamic balance between damage and repair. 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. Methods : Quantitative polymerase chain reaction was used to assess the expression of matrix metalloproteinases (MMPs) and type Ⅰ collagen in HDPCs upon EZH2 and EI1 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. Results :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-κB(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 downregulated the type Ⅰ collagen levels in an experimental model of dental pulpitis in rats. Conclusion: 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 vitro.

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ASH1L Suppresses Matrix Metalloproteinase through Mitogen-activated Protein Kinase Signaling Pathway in Pulpitis

Cited by 15 publications

References 39 publications

EZH2 Promotes Extracellular Matrix Degradation via Nuclear Factor-kB(NF-kB)and p38 signaling Pathways in Pulpitis.

EZH2 Promotes Extracellular Matrix Degradation via Nuclear Factor-kB(NF-kB)and p38 signaling Pathways in Pulpitis.

Bioinformatics Analysis of Gene Expression Profiles for Risk Prediction in Patients with Septic Shock

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

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