Evidence map›Paper›PMID 29540173›Full record

ArticleJournal of biomedical science2018

Adiponectin and adiponectin receptor 1 overexpression enhance inflammatory bowel disease.

Yu-Ju Peng, Tang-Long Shen, Yu-Shan Chen, Harry John Mersmann, Bing-Hsien Liu, Shih-Torng Ding

Open access · diamondAbstract read
In one paragraph

Article in Journal of biomedical science, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
3.6field-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

26 citing papers in PubMed, 46 citations in OpenAlex.

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  15. Role of Adipose Tissue in Inflammatory Bowel Disease.International journal of molecular sciences · 2021
    Review
  16. ROS Dependent Antifungal and Anticancer Modulations ofMolecules (Basel, Switzerland) · 2021
    Article
  17. Review
  18. Article
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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 1 country.

Yu-Ju PengDepartment of Animal Science and Technology, National Taiwan University, No. 50, Ln. 155, Sec. 3, Keelung Rd., Da'an Dist, Taipei City, 10617, Taiwan.
Tang-Long ShenDepartment of Plant Pathology and Microbiology, National Taiwan University, No.1, Sec.4, Roosevelt Road, Taipei, 10617, Taiwan.
Yu-Shan ChenDepartment of Animal Science and Technology, National Taiwan University, No. 50, Ln. 155, Sec. 3, Keelung Rd., Da'an Dist, Taipei City, 10617, Taiwan.
Harry John MersmannDepartment of Animal Science and Technology, National Taiwan University, No. 50, Ln. 155, Sec. 3, Keelung Rd., Da'an Dist, Taipei City, 10617, Taiwan.
Bing-Hsien LiuDepartment of Animal Science and Technology, National Taiwan University, No. 50, Ln. 155, Sec. 3, Keelung Rd., Da'an Dist, Taipei City, 10617, Taiwan.
Shih-Torng DingDepartment of Animal Science and Technology, National Taiwan University, No. 50, Ln. 155, Sec. 3, Keelung Rd., Da'an Dist, Taipei City, 10617, Taiwan. sding@ntu.edu.tw.
National Taiwan University of Science and Technology · TWNational Taiwan University · TW

Funding

Ministry of Science and Technology, Taiwan NSC99-2628-B002-067-MY3
6 · The paper itself

Abstract

backgroundAdiponectin (ADN) is an adipokine derived from adipocytes. It binds to adiponectin receptor 1 and 2 (AdipoR1 and R2) to exert its function in regulating whole-body energy homeostasis and inflammatory responses. However, the role of ADN-AdipoR1 signaling in intestinal inflammation is controversial, and its role in the regulation of neutrophils is still unclear. Our goal was to clarify the role of AdipoR1 signaling in colitis and the effects on neutrophils.

methodsWe generated porcine AdipoR1 transgenic mice (pAdipoR1 mice) and induced murine colitis using dextran sulfate sodium (DSS) to study the potential role of AdipoR1 in inflammatory bowel disease. We also treated a THP-1 macrophage and a HT-29 colon epithelial cell line with ADN recombinant protein to study the effects of ADN on inflammation.

resultsAfter inducing murine colitis, pAdipoR1 mice developed more severe symptoms than wild-type (WT) mice. Treatment with ADN increased the expression of pro-inflammatory factors in THP-1 and HT-29 cells. Moreover, we also observed that the expression of cyclooxygenase2 (cox2), neutrophil chemokines (CXCL1, CXCL2 and CXCL5), and the infiltration of neutrophils were increased in the colon of pAdipoR1 mice.

conclusionsOur study showed that ADN-AdipoR1 signaling exacerbated colonic inflammation through two possible mechanisms. First, ADN-AdipoR1 signaling increased pro-inflammatory factors. Second, AdipoR1 enhanced neutrophil chemokine expression and recruited neutrophils into the colonic tissue to increase inflammation.

Indexed as

Gene ExpressionSignal TransductionAdiponectinAnimalsColitisDextran SulfateFemaleHT29 CellsHumansInflammatory Bowel DiseasesMice, TransgenicReceptors, AdiponectinRecombinant ProteinsSus scrofaTHP-1 CellsAdiponectinADIPOQ protein, humanDextran SulfateReceptors, AdiponectinRecombinant ProteinsAdiponectinAdiponectin receptor 1CXCL1CXCL2CXCL5IBDIl-8Neutrophils

Identifiers

PMID29540173
PMCPMC5851065
OpenAlexW2800569054

What OpenQuestion holds

Textmetadata
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.