Evidence map›Paper›PMID 32211804›Full record

ArticleBioscience reports2020

miR-802 participates in the inflammatory process of inflammatory bowel disease by suppressing SOCS5.

Jun Yao, Ruoyu Gao, Minghan Luo, Defeng Li, Liliangzi Guo, Zichao Yu, Feng Xiong, Cheng Wei, Benhua Wu, Zhenglei Xu and 3 more

RetractedOpen access · goldAbstract readRetracted Publication
In one paragraph

Article in Bioscience reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 6 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed, 1 pooled it
0.6field-weighted citation impact, top 39% 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

6 citing papers in PubMed, 1 synthesis or guideline pooled it, 10 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. AdipocyteeLife · 2024
    Article
  4. Article
  5. Article
  6. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors at 2 institutions in 1 country.

Jun YaoDepartment of Gastroenterology, Jinan University of Second Clinical Medical Sciences, Shenzhen Municipal People's Hospital, No. 1017, East Gate Road, Shenzhen City, Guangdong Province 518020, China.
Ruoyu GaoDepartment of Gastroenterology, Jinan University of Second Clinical Medical Sciences, Shenzhen Municipal People's Hospital, No. 1017, East Gate Road, Shenzhen City, Guangdong Province 518020, China.
Minghan LuoDepartment of Gastroenterology, Jinan University of Second Clinical Medical Sciences, Shenzhen Municipal People's Hospital, No. 1017, East Gate Road, Shenzhen City, Guangdong Province 518020, China.
Defeng LiDepartment of Gastroenterology, Jinan University of Second Clinical Medical Sciences, Shenzhen Municipal People's Hospital, No. 1017, East Gate Road, Shenzhen City, Guangdong Province 518020, China.
Liliangzi GuoDepartment of Gastroenterology, Jinan University of Second Clinical Medical Sciences, Shenzhen Municipal People's Hospital, No. 1017, East Gate Road, Shenzhen City, Guangdong Province 518020, China.
Zichao YuDepartment of Gastroenterology, Jinan University of Second Clinical Medical Sciences, Shenzhen Municipal People's Hospital, No. 1017, East Gate Road, Shenzhen City, Guangdong Province 518020, China.
Feng XiongDepartment of Gastroenterology, Jinan University of Second Clinical Medical Sciences, Shenzhen Municipal People's Hospital, No. 1017, East Gate Road, Shenzhen City, Guangdong Province 518020, China.
Cheng WeiDepartment of Gastroenterology, Jinan University of Second Clinical Medical Sciences, Shenzhen Municipal People's Hospital, No. 1017, East Gate Road, Shenzhen City, Guangdong Province 518020, China.
Benhua WuDepartment of Gastroenterology, Jinan University of Second Clinical Medical Sciences, Shenzhen Municipal People's Hospital, No. 1017, East Gate Road, Shenzhen City, Guangdong Province 518020, China.
Zhenglei XuDepartment of Gastroenterology, Jinan University of Second Clinical Medical Sciences, Shenzhen Municipal People's Hospital, No. 1017, East Gate Road, Shenzhen City, Guangdong Province 518020, China.
Dingguo ZhangDepartment of Gastroenterology, Jinan University of Second Clinical Medical Sciences, Shenzhen Municipal People's Hospital, No. 1017, East Gate Road, Shenzhen City, Guangdong Province 518020, China.
Jianyao WangDepartment of General Surgery, Shenzhen Children's Hospital, No. 7019, Yitian Road Road, Shenzhen City, Guangdong Province 518026, China.
Lisheng WangDepartment of Gastroenterology, Jinan University of Second Clinical Medical Sciences, Shenzhen Municipal People's Hospital, No. 1017, East Gate Road, Shenzhen City, Guangdong Province 518020, China.
Jinan University · CNShenzhen Children's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The present study aims to reveal the detailed molecular mechanism of microRNA (miR)-802 in the progression of inflammatory bowel disease (IBD). IBD tissues were obtained from IBD patients, followed by CD4+ cells isolation. Then, qRT-PCR and ELISA were used to detect the expression of miR-802, suppressor of cytokine signaling 5 (SOCS5), interleukin (IL)-17A and tumor necrosis factor (TNF)-α. Transfection of miR-802 mimics and miR-802 inhibitor in CD4+ cells was detected by Western blot. TargetScan and luciferase reporter assay were used to detect the relationship between SOCS5 and miR-802. Finally, colitis mice model was established to verify whether miR-802 inhibitor was involved in the protective effect of colonic mucosa. The miR-802 was highly expressed in inflamed mucosa and PBMC cells of IBD. The highest expression of miR-802 was observed in CD4+ T cells based on different immune cell subsets analysis. SOCS5 was the target gene of miR-802. The mice model experiments showed that blockade of miR-802 could alleviate mice colitis. Our study suggests that up-regulation of miR-802 plays an important role in inflammatory process of IBD via targeting SOCS5. Moreover, the differentiation of Th17 and secretion of TNF-α in IBD could be stimulated by miR-802.

Indexed as

AdultAnimalsCase-Control StudiesCD4-Positive T-LymphocytesCell DifferentiationCells, CulturedColitis, UlcerativeColonCrohn DiseaseDisease Models, AnimalFemaleHealthy VolunteersHumansInterleukin-17Intestinal MucosaMaleIL17A protein, humanInterleukin-17MicroRNAsMIRN802 microRNA, humanMIRN802 microRNA, mouseSOCS5 protein, humanSuppressor of Cytokine Signaling ProteinsTNF protein, humanTrinitrobenzenesulfonic AcidTumor Necrosis Factor-alphainflammatory bowel diseasemice colitis modelmiR-802SOCS5Th17TNF-α

Identifiers

PMID32211804
PMCPMC7138906
OpenAlexW3013440205

What Socratic 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 Socratic graph.