Evidence map›Paper›PMID 33332758›Full record

ArticleImmunity, inflammation and disease2021

miR-223 improves intestinal inflammation through inhibiting the IL-6/STAT3 signaling pathway in dextran sodium sulfate-induced experimental colitis.

Juanjuan Zhang, Chenyang Wang, Zhen Guo, Binlin Da, Weiming Zhu, Qiurong Li

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Immunity, inflammation and disease, 2021. 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 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.6field-weighted citation impact, top 15% 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

21 citing papers in PubMed, 29 citations in OpenAlex.

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  14. Sympathetic nerve-adipocyte interactions in response to acute stress.Journal of molecular medicine (Berlin, Germany) · 2022
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Juanjuan ZhangResearch Institute of General Surgery, Jinling Hospital, Nanjing Medical University, Nanjing, Jiangsu, China.
Chenyang WangResearch Institute of General Surgery, Jinling Hospital, Nanjing, Jiangsu, China.
Zhen GuoResearch Institute of General Surgery, Jinling Hospital, Nanjing, Jiangsu, China.
Binlin DaResearch Institute of General Surgery, Jinling Hospital, Nanjing, Jiangsu, China.
Weiming ZhuResearch Institute of General Surgery, Jinling Hospital, Nanjing Medical University, Nanjing, Jiangsu, China.
Qiurong LiResearch Institute of General Surgery, Jinling Hospital, Nanjing Medical University, Nanjing, Jiangsu, China.ORCID 0000-0002-5470-3161
Nanjing General Hospital of Nanjing Military Command · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionThe pathogenesis of inflammatory bowel disease (IBD) has not yet been clarified and is closely related to several pro-inflammatory factors. MicroRNA-233 (miR-223) might be involved in the development of IBD; however, the mechanism underlying its pathogenesis is unclear. In this study, we attempted to determine the role of miR-223 in dextran sodium sulfate (DSS)-induced colitis and explore the involvement of the IL-6/STAT3 pathway in the development of intestinal mucosal inflammation. MATERIALS AND

methodsExcept control (WT) group, male C57BL/6 mice were provided DSS, then treated for with miR-223 agomir or antagomir including DSS group, DSS + miR-223 agomir (DSS + A) group, and DSS + miR-223 antagomir (DSS + AN) group. The colitis symptoms were observed, the disease activity index (DAI) score were recorded daily, and colonic inflammation was evaluated by histopathological scoring. The expression of myeloperoxidase (MPO), cytokines and IL-6/STAT3 pathway-related proteins were measured.

resultsmiR-223 expression in the terminal ileum and colon was increased in the DSS group compared with the WT group. Colitis symptoms were significantly alleviated in the DSS + A group and exacerbated in the DSS + AN group after administration of the miR-223 agomir and antagomir, respectively. MPO, tumor necrosis factor-α, IL-6, and IL-17 were decreased and IL-10 was increased in the DSS + A group, but these changes were reversed in the DSS + AN group. Gp130, p-STAT3, Bcl-2, and Bcl-xl in the colon declined in the DSS + A group, but these levels increased in the DSS + AN group.

conclusionsThe upregulation of miR-223 by agomir administration alleviated colonic inflammation in a DSS-induced colitis model, which was likely mediated by inhibiting the production of pro-inflammatory cytokines via the IL-6/STAT3 signaling pathway. These findings provide evidence that miR-223 might have potential therapeutic implications in IBD.

Indexed as

ColitisMicroRNAsAnimalsDextran SulfateDisease Models, AnimalInflammationInterleukin-6MaleMiceMice, Inbred C57BLSignal TransductionSulfatesDextran SulfateInterleukin-6MicroRNAsMIRN223 microRNA, mousesodium sulfateSulfatescytokinesdextran sodium sulfate-induced colitisIL-6/STAT3 signaling pathwayinflammatory bowel diseasemiR-223

Identifiers

PMID33332758
PMCPMC7860526
OpenAlexW3111638109

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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.