Evidence map›Paper›PMID 34112215›Full record

ArticleClinical epigenetics2021

STAT1 epigenetically regulates LCP2 and TNFAIP2 by recruiting EP300 to contribute to the pathogenesis of inflammatory bowel disease.

Ya-Li Yu, Meng Chen, Hua Zhu, Ming-Xing Zhuo, Ping Chen, Yu-Juan Mao, Lian-Yun Li, Qiu Zhao, Min Wu, Mei Ye

Open access · goldAbstract read
In one paragraph

Article in Clinical epigenetics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.1field-weighted citation impact, top 7% 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

23 citing papers in PubMed, 43 citations in OpenAlex.

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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

10 authors at 1 institution in 1 country.

Ya-Li YuDepartment of Gastroenterology, Zhongnan Hospital, Wuhan University, Wuhan, 430071, Hubei, China.
Meng ChenDepartment of Gastroenterology, Zhongnan Hospital, Wuhan University, Wuhan, 430071, Hubei, China.
Hua ZhuDepartment of Gastroenterology, Zhongnan Hospital, Wuhan University, Wuhan, 430071, Hubei, China.
Ming-Xing ZhuoDepartment of Gastroenterology, Zhongnan Hospital, Wuhan University, Wuhan, 430071, Hubei, China.
Ping ChenDepartment of Gastroenterology, Zhongnan Hospital, Wuhan University, Wuhan, 430071, Hubei, China.
Yu-Juan MaoDepartment of Gastroenterology, Zhongnan Hospital, Wuhan University, Wuhan, 430071, Hubei, China.
Lian-Yun LiFrontier Science Center for Immunology and Metabolism, Hubei Key Laboratory of Cell Homeostasis, Hubei Key Laboratory of Developmentally Originated Disease, Hubei Key Laboratory of Intestinal and Colorectal Diseases, College of Life Sciences, Wuhan University, Wuhan, 430072, Hubei, China.
Qiu ZhaoDepartment of Gastroenterology, Zhongnan Hospital, Wuhan University, Wuhan, 430071, Hubei, China.
Min WuFrontier Science Center for Immunology and Metabolism, Hubei Key Laboratory of Cell Homeostasis, Hubei Key Laboratory of Developmentally Originated Disease, Hubei Key Laboratory of Intestinal and Colorectal Diseases, College of Life Sciences, Wuhan University, Wuhan, 430072, Hubei, China.
Mei YeDepartment of Gastroenterology, Zhongnan Hospital, Wuhan University, Wuhan, 430071, Hubei, China. wumeiye08@163.com.ORCID 0000-0002-9393-3680
Wuhan University · CN

Funding

National Natural Science Foundation of China No.81870391
6 · The paper itself

Abstract

backgroundThe aetiology of inflammatory bowel disease (IBD) is related to genetics and epigenetics. Epigenetic regulation of the pathogenesis of IBD has not been well defined. Here, we investigated the role of H3K27ac events in the pathogenesis of IBD. Based on previous ChIP-seq and RNA-seq assays, we studied signal transducer and activator of transcription 1 (STAT1) as a transcription factor (TF) and investigated whether the STAT1-EP300-H3K27ac axis contributes to the development of IBD. We performed ChIP-PCR to investigate the interaction between STAT1 and H3K27ac, and co-IP assays were performed to investigate the crosstalk between STAT1 and EP300.

resultsLymphocyte cytosolic protein 2 (LCP2) and TNF-α-inducible protein 2 (TNFAIP2) are target genes of STAT1. p-STAT1 binds to the enhancer loci of the two genes where H3K27ac is enriched, and EP300 subsequently binds to regulate their expression. In mice with dextran sulfate sodium (DSS)-induced acute colitis, an EP300 inhibitor significantly inhibited colitis.

conclusionsp-STAT1 and EP300 promote TNFAIP2 and LCP2 expression through an increase in H3K27ac enrichment on their enhancers and contribute to the pathogenesis of chronic inflammation.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsChinaCytokinesDisease Models, AnimalDNA MethylationE1A-Associated p300 ProteinEpigenesis, GeneticHumansInflammatory Bowel DiseasesMicePhosphoproteinsSTAT1 Transcription FactorAdaptor Proteins, Signal TransducingCytokinesE1A-Associated p300 ProteinEP300 protein, humanPhosphoproteinsSLP-76 signal Transducing adaptor proteinsSTAT1 protein, humanSTAT1 Transcription FactorTNFAIP2 protein, humanEnhancerEP300H3K27acIBDSTAT1

Identifiers

PMID34112215
PMCPMC8194145
OpenAlexW3166451419

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Registered trials

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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.