Evidence map›Paper›PMID 32057181›Full record

ArticleJournal of cellular and molecular medicine2020

FoxO1 regulates TLR4/MyD88/MD2-NF-κB inflammatory signalling in mucosal barrier injury of inflammatory bowel disease.

Chenyang Han, Li Guo, Yongjia Sheng, Yi Yang, Jin Wang, Yanling Gu, Wenyan Li, Xiaohong Zhou, Qingcai Jiao

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

18 citing papers in PubMed, 32 citations in OpenAlex.

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  12. Journal of cellular and molecular medicine · 2022
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4 · The record

Corrections and comments

  • Erratum issued
    2022
5 · Who and what money

Authors and funding

9 authors at 2 institutions in 1 country.

Chenyang HanState Key Laboratory of Pharmaceutical Biotechnology, School of Life Science, Nanjing University, Nanjing, China.ORCID 0000-0002-2805-580X
Li GuoDepartment of Center Laboratory, The Second Affiliated Hospital of Jiaxing University, Jiaxing, China.
Yongjia ShengDepartment of pharmacy, The Second Affiliated Hospital of Jiaxing University, Jiaxing, China.
Yi YangDepartment of pharmacy, The Second Affiliated Hospital of Jiaxing University, Jiaxing, China.
Jin WangDepartment of pharmacy, The Second Affiliated Hospital of Jiaxing University, Jiaxing, China.
Yanling GuDepartment of pharmacy, The Second Affiliated Hospital of Jiaxing University, Jiaxing, China.
Wenyan LiDepartment of pharmacy, The Second Affiliated Hospital of Jiaxing University, Jiaxing, China.
Xiaohong ZhouDepartment of gastroenterology, The Second Affiliated Hospital of Jiaxing University, Jiaxing, China.
Qingcai JiaoState Key Laboratory of Pharmaceutical Biotechnology, School of Life Science, Nanjing University, Nanjing, China.
Jiaxing University · CNNanjing University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In this study, FoxO1 transgenic mice (transgenic, FoxO1-Tg) and C57BL/6 wild-type (wild-type, FoxO1-WT) mice were used to establish chronic colitis by drinking water containing dextran sulphate sodium (DSS). Afterwards, we observed the life changes in mice and assessed the pathological changes by H&E tissue staining. In addition, the TLR4/MyD88/MD2-NF-κB inflammatory signals were detected. As a result, under DSS treatment, the activation level of TLR4/MyD88/MD2-NF-κB inflammatory signal was higher in FoxO1-Tg mice than that in FoxO1-WT mice. Meanwhile, the intestinal mucosal tissue damage was more severe, the down-regulation of tight junction protein level was more significant and the life quality was decreased to a higher degree in FoxO1-Tg mice compared with those in FoxO1-WT mice. Caco-2 cells were used to mimic the intestinal mucosal barrier model for in vitro assays. In addition, lentiviral packaging FoxO1 overexpressing plasmid was transfected into Caco-2 cells for FoxO1 overexpression. TNF-α intervention was performed for intestinal mucosal inflammatory response model. Consequently, the down-regulation of FoxO1 inhibited the activation of TLR4/MyD88/MD2-NF-κB inflammatory signal, decreased the mucosal barrier permeability and up-regulated the expression of tight junction protein. By contrast, the overexpression of FoxO1 increased the mucosal barrier permeability and down-regulated the level of tight junction protein.

Indexed as

AdultAgedAnimalsBody WeightCaco-2 CellsCell LineCell Membrane PermeabilityChronic DiseaseColitisDown-RegulationFemaleForkhead Box Protein O1HumansInflammationInflammatory Bowel DiseasesIntestinal MucosaForkhead Box Protein O1FOXO1 protein, humanFoxo1 protein, mouseLymphocyte Antigen 96Myeloid Differentiation Factor 88NF-kappa BRNA, Small InterferingTight Junction ProteinsToll-Like Receptor 4inflammatory bowel diseaseinflammatory signaltight junctiontranscription factor FoxO1

Identifiers

PMID32057181
PMCPMC7131908
OpenAlexW3005731808

What OpenQuestion holds

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LicenceCC BY
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.