Evidence map›Paper›PMID 31273598›Full record

ArticleDigestive diseases and sciences2019

EZH2 Regulates Intestinal Inflammation and Necroptosis Through the JNK Signaling Pathway in Intestinal Epithelial Cells.

Xinhe Lou, Huatuo Zhu, Longgui Ning, Chunxiao Li, Sha Li, Haojie Du, Xinxin Zhou, Guoqiang Xu

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In one paragraph

Article in Digestive diseases and sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 1 pooled it
2.2field-weighted citation impact, top 11% 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

30 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.

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  13. Necroptosis in inflammatory bowel disease: A potential effective target.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2022
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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

8 authors at 2 institutions in 1 country.

Xinhe LouDepartment of Gastroenterology, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, 310003, China.
Huatuo ZhuDepartment of Gastroenterology, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, 310003, China.
Longgui NingDepartment of Gastroenterology, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, 310003, China.
Chunxiao LiDepartment of Gastroenterology, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, 310003, China.
Sha LiDepartment of Gastroenterology, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, 310003, China.
Haojie DuDepartment of Gastroenterology, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, 310003, China.
Xinxin ZhouDepartment of Gastroenterology, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, 310003, China.
Guoqiang XuDepartment of Gastroenterology, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, 310003, China. 1193065@zju.edu.cn.ORCID http://orcid.org/0000-0003-1337-9120
Zhejiang University · CNFirst Affiliated Hospital Zhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundInflammatory bowel disease (IBD) is a common disorder of chronic intestinal inflammation that can be caused by the disruption of intestinal immune homeostasis.

aimWe aimed to evaluate the role of enhancer of zeste homolog 2 (EZH2) in the inflammatory response and explore the association between EZH2 and necroptosis in human epithelial colorectal adenocarcinoma cell lines.

methodsIn both in vitro and in vivo models, expression of EZH2 in intestinal tissues was verified by histology. The expression of inflammatory cytokines in cell lines treated with EZH2 siRNA with or without stimulus was analyzed by quantitative real-time polymerase chain reaction. An intestinal necroptosis cell model was established to elucidate whether EZH2 is involved in necroptosis.

resultsOur present data indicated that EZH2 expression was decreased in in vitro and in vivo models and in patients with inflammatory bowel disease. EZH2 downregulation increased the expression of inflammatory factors, including TNF-α, IL-8, IL-17, CCL5, and CCL20 in a Caco-2 cell model. The JNK pathway was activated with the reduction of EZH2. In the necroptosis model, downregulation of EZH2 was detected with the upregulation of necroptotic markers RIP1 and RIP3. In addition, EZH2 knockdown with siRNA increased p-JNK and p-c-Jun.

conclusionOur data suggest that EZH2 plays an important role in the development of intestinal inflammation and necroptosis. Hence, EZH2 could be a potential therapeutic target for IBD.

Indexed as

AnimalsCaco-2 CellsChemokine CCL20Chemokine CCL5ColitisColitis, UlcerativeCrohn DiseaseDextran SulfateDown-RegulationEnhancer of Zeste Homolog 2 ProteinGene Knockdown TechniquesHumansInflammationInflammatory Bowel DiseasesInterleukin-17Interleukin-8AGFG1 protein, humanCCL20 protein, humanCCL5 protein, humanChemokine CCL20Chemokine CCL5CXCL8 protein, humanDextran SulfateEnhancer of Zeste Homolog 2 ProteinEZH2 protein, humanEzh2 protein, mouseInterleukin-17Interleukin-8JNK Mitogen-Activated Protein KinasesNuclear Pore Complex ProteinsPhosphoproteinsProto-Oncogene Proteins c-junReceptor-Interacting Protein Serine-Threonine KinasesRIPK3 protein, humanRNA-Binding ProteinsTNF protein, humanTrinitrobenzenesulfonic AcidTumor Necrosis Factor-alphaEZH2Intestinal inflammationJNK/AP-1 pathwayNecroptosis

Identifiers

PMID31273598
OpenAlexW2955675764

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.