Evidence map›Paper›PMID 28205598›Full record

ArticleScientific reports2017

Lyn regulates mucus secretion and MUC5AC via the STAT6 signaling pathway during allergic airway inflammation.

Xiaoyun Wang, Yin Li, Deyu Luo, Xing Wang, Yun Zhang, Zhigang Liu, Nanshan Zhong, Min Wu, Guoping Li

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
3.1field-weighted citation impact, top 8% 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

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 49 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

9 authors at 5 institutions in 2 countries.

Xiaoyun WangInflammation &Allergic Diseases Research Unit, Affiliated Hospital of Southwest Medical University, Luzhou 646000, Sichuan, China.
Yin LiThe First Clinic College, Chongqing Medical University, Chongqing 401331, China.
Deyu LuoInflammation &Allergic Diseases Research Unit, Affiliated Hospital of Southwest Medical University, Luzhou 646000, Sichuan, China.
Xing WangInflammation &Allergic Diseases Research Unit, Affiliated Hospital of Southwest Medical University, Luzhou 646000, Sichuan, China.
Yun ZhangInflammation &Allergic Diseases Research Unit, Affiliated Hospital of Southwest Medical University, Luzhou 646000, Sichuan, China.
Zhigang LiuState Key Laboratory of Respiratory Disease for Allergy at Shenzhen University, School of Medicine, Shenzhen University, Nanhai Ave 3688, Shenzhen Guangdong 518060, P.R. China.
Nanshan ZhongState Key Laboratories of Respiratory Disease, Ghuangzhou Medical University, Guangdong 510120, P.R. China.
Min WuDepartment of Basic Biomedical Sciences, School of Medicine and Health Sciences, University of North Dakota, 501 N Columbia Rd, Grand Forks, ND 58203-9037, USA.
Guoping LiInflammation &Allergic Diseases Research Unit, Affiliated Hospital of Southwest Medical University, Luzhou 646000, Sichuan, China.
Affiliated Hospital of Southwest Medical University · CNChongqing Medical University · CNShenzhen University · CNState Key Laboratory of Respiratory Disease · CNUniversity of North Dakota · US

Funding

Lung innate immunity against bacterial infectionR01AI109317 · NIAID · UNIVERSITY OF NORTH DAKOTA · PI WU, MIN · 2014 to 2018
$1.7M
NIAID NIH HHS R01 AI109317
6 · The paper itself

Abstract

Hypersecretion of mucus is an important component of airway remodeling and contributes to the mucus plugs and airflow obstruction associated with severe asthma phenotypes. Lyn has been shown to down-regulate allergen-induced airway inflammation. However, the role of Lyn in mucin gene expression remains unresolved. In this study, we first demonstrate that Lyn overexpression decreased the mucus hypersecretion and levels of the muc5ac transcript in mice exposed to ovalbumin (OVA). Lyn overexpression also decreased the infiltration of inflammatory cells and the levels of IL-13 and IL-4 in OVA-challenged airways. Whereas Lyn knockdown increased the IL-4 or IL-13-induced MUC5AC transcript and protein levels in the human bronchial epithelial cell line, 16HBE, Lyn overexpression decreased IL-4- or IL-13-induced MUC5AC transcript and protein levels. Overexpression of Lyn also decreased the expression and phosphorylation of STAT6 in OVA-exposed mice, whereas Lyn knockdown increased STAT6 and MUC5AC levels in 16HBE cells. Finally, chromatin immunoprecipitation analysis confirmed that Lyn overexpression decreased the binding of STAT6 to the promoter region of Muc5ac in mice exposed to OVA. Collectively, these findings demonstrated that Lyn overexpression ameliorated airway mucus hypersecretion by down-regulating STAT6 and its binding to the MUC5AC promoter.

Indexed as

Signal TransductionAnimalsCytokinesDisease Models, AnimalGene ExpressionHumansMiceMice, KnockoutModels, BiologicalMucin 5ACMucusOvalbuminPromoter Regions, GeneticProtein BindingRespiratory HypersensitivityRespiratory MucosaCytokineslyn protein-tyrosine kinaseMUC5AC protein, humanMucin 5ACOvalbuminsrc-Family KinasesSTAT6 protein, humanSTAT6 Transcription Factor

Identifiers

PMID28205598
PMCPMC5312001
OpenAlexW2587865736

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.