Evidence map›Paper›PMID 32209121›Full record

ArticleBiological research2020

Mast cells-derived MiR-223 destroys intestinal barrier function by inhibition of CLDN8 expression in intestinal epithelial cells.

Musheng Li, Junhong Zhao, Meiwan Cao, Ruitao Liu, Guanhua Chen, Songyu Li, Yuanwen Xie, Jing Xie, Yang Cheng, Ling Huang and 7 more

Open access · goldAbstract read
In one paragraph

Article in Biological research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
4.1field-weighted citation impact, top 5% 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

53 citing papers in PubMed, 85 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

17 authors at 6 institutions in 2 countries.

Musheng LiDepartment of Gastroenterology, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, 510623, China.
Junhong ZhaoDepartment of Gastroenterology, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, 510623, China.
Meiwan CaoDepartment of Gastroenterology, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, 510623, China.
Ruitao LiuDepartment of Gastroenterology, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, 510623, China.
Guanhua ChenDepartment of Gastroenterology, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, 510623, China.
Songyu LiDepartment of Clinical Laboratory, Qionghai Hospital of Traditional Chinese Medicine, Qionghai, 571400, China.
Yuanwen XieDepartment of Anorectal, Qionghai Hospital of Traditional Chinese Medicine, Qionghai, 571400, China.
Jing XieDepartment of Gastroenterology, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, 510623, China.
Yang ChengDepartment of Gastroenterology, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, 510623, China.
Ling HuangDepartment of Gastroenterology, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, 510623, China.
Mingmin SuDepartment of Cancer Biology and Therapeutics, School of Pharmacy and Pharmaceutical Sciences, Cardiff University, Wales, CF103AT, UK.
Yuxin XuDepartment of Preventive Medicine, School of School of Public Health, Fujian Medical University, Fuzhou, 350122, China.
Mingyue ZhengSchool of Marine Life Sciences, Ocean University of China, Qingdao, Shandong, 266003, China.
Kejian ZouDepartment of General Surgery, Hainan General Hospital, Haikou, China.
Lanlan GengDepartment of Gastroenterology, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, 510623, China. genglan_2001@hotmail.com.
Wanfu XuDepartment of Gastroenterology, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, 510623, China. xushi123@gmail.com.ORCID http://orcid.org/0000-0002-1467-9830
Sitang GongDepartment of Gastroenterology, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, 510623, China. gongsitang@hotmail.com.
Guangzhou Medical University · CNGuangzhou Women and Children Medical Center · CNCardiff University · GBFujian Medical University · CNHainan General Hospital · CNOcean University of China · CN

Funding

Clinical key specialty and construction of cultivate the key subject of Guangzhou Women and Children's Medical Center No.170000105)Funding of cooperation projects between Guangzhou Women and Children's Medical Center and Sun Yat-Sen University No.201704020223Funding of Guangzhou Institute of Pediatrics/Guangzhou Women and Children's Medical Center No.IP-2018-009Funding of Guangzhou Institute of Pediatrics/Guangzhou Women and Children's Medical Center Pre-NSFC-2019-005Guangzhou Municipal Health and Family Planning Commission No.20191A010024Guangzhou Municipal Science and Technology Project No.201804010148Guangzhou Municipal Science and Technology Project No.201904010485high-level talents of hainan natural science foundation No.2019RC366Medical Science and Technology Foundation of Guangdong Province (CN) No.A2018395National Natural Science Foundation of China No.81770552National Natural Science Foundation of China No.81860101Natural Science Foundation of Guangdong Province No.2017A030313838Natural Science Foundation of Guangdong Province No.2018A0303130175Natural Science Foundation of Hainan Province No.2819QN372unding of Guangzhou Institute of Pediatrics/Guangzhou Women and Children's Medical Center No.IP-2016-005
6 · The paper itself

Abstract

backgroundMast cells (MCs) have been found to play a critical role during development of inflammatory bowel disease (IBD) that characterized by dysregulation of inflammation and impaired intestinal barrier function. However, the function of MCs in IBD remains to be fully elucidated.

resultsIn our study, we used exosomes isolated from human mast cells-1 (HMCs-1) to culture with NCM460, HT-29 or CaCO2 of intestinal epithelial cells (IECs) to investigate the communication between MCs and IECs. We found that MCs-derived exosomes significantly increased intestinal epithelial permeability and destroyed intestinal barrier function, which is attributed to exosome-mediated functional miRNAs were transferred from HMCs-1 into IECs, leading to inhibit tight junction-related proteins expression, including tight junction proteins 1 (TJP1, ZO-1), Occludin (OCLN), Claudin 8 (CLDN8). Microarray and bioinformatic analysis have further revealed that a panel of miRNAs target different tight junction-related proteins. Interestingly, miR-223 is enriched in mast cell-derived exosome, which inhibit CLDN8 expression in IECs, while treatment with miR-223 inhibitor in HT-29 cells significantly reversed the inhibitory effect of HMCs-1-derived exosomes on CLDN 8 expression. Most importantly, enrichment of MCs accumulation in intestinal mucosa of patients with IBD compared with those healthy control.

conclusionsThese results indicated that enrichment of exosomal miR-223 from HMCs-1 inhibited CLDN8 expression, leading to destroy intestinal barrier function. These finding provided a novel insight of MCs as a new target for therapeutic treatment of IBD.

Indexed as

AnimalsCaco-2 CellsCattleCells, CulturedClaudinsComputational BiologyEpithelial CellsExosomesHumansInflammatory Bowel DiseasesIntestinal MucosaMast CellsMicroRNAsOccludinPermeabilityTissue Array Analysisclaudin 8ClaudinsMicroRNAsMIR223, humanOccludinZonula Occludens-1 ProteinClaudin 8ExosomesInflammatory bowel diseaseMast cellsmiR-223

Identifiers

PMID32209121
PMCPMC7092522
OpenAlexW3012978815

What OpenQuestion holds

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LicenceCC BY
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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.