Evidence map›Paper›PMID 33884563›Full record

ArticleInflammation2021

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

Jie He, Man Qin, Yingyi Chen, Ziqi Hu, Ling Ye, Tianqian Hui

Abstract read
PubMed Publisher
In one paragraph

Article in Inflammation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.2field-weighted citation impact, top 23% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

5 citing papers in PubMed, 11 citations in OpenAlex.

  1. Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 2 countries.

Jie HeDepartment of Pediatric Dentistry, Central Laboratory, Peking University School and Hospital of Stomatology & National Center of Stomatology &National Clinical Research Center for Oral Diseases & National Engineering Laboratory for Digital and Material Technology of Stomatology, No.22, Zhongguancun South Avenue, Haidian District, Beijing, 100081, PR, China.ORCID https://orcid.org/0000-0001-9864-4397
Man QinDepartment of Pediatric Dentistry, Central Laboratory, Peking University School and Hospital of Stomatology & National Center of Stomatology &National Clinical Research Center for Oral Diseases & National Engineering Laboratory for Digital and Material Technology of Stomatology, No.22, Zhongguancun South Avenue, Haidian District, Beijing, 100081, PR, China. qin-man@foxmail.com.ORCID https://orcid.org/0000-0001-5791-3319
Yingyi ChenDepartment of Pediatric Dentistry, Central Laboratory, Peking University School and Hospital of Stomatology & National Center of Stomatology &National Clinical Research Center for Oral Diseases & National Engineering Laboratory for Digital and Material Technology of Stomatology, No.22, Zhongguancun South Avenue, Haidian District, Beijing, 100081, PR, China.ORCID https://orcid.org/0000-0003-4875-244X
Ziqi HuDepartment of Pediatric Dentistry, Central Laboratory, Peking University School and Hospital of Stomatology & National Center of Stomatology &National Clinical Research Center for Oral Diseases & National Engineering Laboratory for Digital and Material Technology of Stomatology, No.22, Zhongguancun South Avenue, Haidian District, Beijing, 100081, PR, China.ORCID https://orcid.org/0000-0001-9412-2663
Ling YeState Key Laboratory of Oral Diseases, West China Hospital of Stomatology, Sichuan University, Sichuan, China.ORCID http://orcid.org/0000-0001-5469-0017
Tianqian HuiDepartment of Pediatric Dentistry, Central Laboratory, Peking University School and Hospital of Stomatology & National Center of Stomatology &National Clinical Research Center for Oral Diseases & National Engineering Laboratory for Digital and Material Technology of Stomatology, No.22, Zhongguancun South Avenue, Haidian District, Beijing, 100081, PR, China. huitianqian@sina.com.ORCID http://orcid.org/0000-0002-4359-211X
Peking University · CNSichuan University · CN

Funding

Natural Science Foundation of China 81800959
6 · The paper itself

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.

Indexed as

AnimalsCells, CulturedDental PulpEnhancer of Zeste Homolog 2 ProteinExtracellular MatrixHumansMaleMAP Kinase Signaling SystemNF-kappa BPulpitisRatsRats, Sprague-DawleyEnhancer of Zeste Homolog 2 ProteinEZH2 protein, humanNF-kappa Bextracellular matrixEZH2nuclear factor-κBP38pulpitis

Identifiers

PMID33884563
OpenAlexW3119917585

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.