Evidence map›Paper›PMID 25889697›Full record

ArticleRespiratory research2015

IL-25 induces airways angiogenesis and expression of multiple angiogenic factors in a murine asthma model.

Xiujuan Yao, Wei Wang, Yan Li, Ping Huang, Qian Zhang, Jingjing Wang, Wen Wang, Zhe Lv, Yunqing An, Jianguo Qin and 4 more

Open access · goldAbstract readComparative Study
In one paragraph

Article in Respiratory research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.9field-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

17 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
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  8. Article
  9. Review
  10. Frontiers in immunology · 2021
    Article
  11. Article
  12. Angiogenesis in the lung.The Journal of physiology · 2019
    Review
  13. Review
  14. Review
  15. 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

14 authors at 4 institutions in 2 countries.

Xiujuan YaoDepartment of Respiratory Medicine, Beijing Tongren Hospital, Capital Medical University, Beijing, People's Republic of China. yaoxiujuanhello@163.com.
Wei WangDepartment of Immunology, School of Basic Medical Sciences, Capital Medical University, Beijing, People's Republic of China. wy_robin@ccmu.edu.cn.
Yan LiDepartment of Respiratory and Critical Care Medicine, Beijing Chao-Yang Hospital, Capital Medical University & Beijing Institute of Respiratory Medicine, Beijing, People's Republic of China. liyanok@126.com.
Ping HuangDepartment of Immunology, School of Basic Medical Sciences, Capital Medical University, Beijing, People's Republic of China. 317144227@qq.com.
Qian ZhangDepartment of Respiratory Medicine, Beijing Tongren Hospital, Capital Medical University, Beijing, People's Republic of China. zqjy0405@163.com.
Jingjing WangDepartment of Laboratory Animal Sciences, Capital Medical University, Beijing, People's Republic of China. wangjj@ccmu.edu.cn.
Wen WangDepartment of Respiratory and Critical Care Medicine, Beijing Chao-Yang Hospital, Capital Medical University & Beijing Institute of Respiratory Medicine, Beijing, People's Republic of China. wenwang318@126.com.
Zhe LvDepartment of Immunology, School of Basic Medical Sciences, Capital Medical University, Beijing, People's Republic of China. lvzhe327@ccmu.edu.cn.
Yunqing AnDepartment of Immunology, School of Basic Medical Sciences, Capital Medical University, Beijing, People's Republic of China. anyunq@ccmu.edu.cn.
Jianguo QinDongfang Hospital, The Second Clinical Medical College of Beijing University of Chinese Medicine, Beijing, People's Republic of China. qindoctor@163.com.
Chris J CorriganKing's College London, MRC & Asthma UK Centre in Allergic Mechanisms of Asthma, Division of Asthma, Allergy & Lung Biology, London, UK. chris.corrigan@kcl.ac.uk.
Kewu HuangDepartment of Respiratory and Critical Care Medicine, Beijing Chao-Yang Hospital, Capital Medical University & Beijing Institute of Respiratory Medicine, Beijing, People's Republic of China. kewuhuang@126.com.
Yongchang SunDepartment of Respiratory Medicine, Beijing Tongren Hospital, Capital Medical University, Beijing, People's Republic of China. suny@ccmu.edu.cn.
Sun YingDepartment of Immunology, School of Basic Medical Sciences, Capital Medical University, Beijing, People's Republic of China. ying.sun@kcl.ac.uk.
Capital Medical University · CNAsthma UK · GBBeijing Chao-Yang Hospital · CNBeijing University of Chinese Medicine · CN

Funding

Medical Research Council G1000758
6 · The paper itself

Abstract

backgroundTh2-promoting cytokine IL-25 might contribute to bronchial mucosal vascular remodelling in asthma through its receptor expressed by vascular endothelial and vascular smooth muscle cells.

methodsBy utilising a newly established chronic asthma murine model induced by direct exposure of the airways to IL-25 alone, we examined effects of IL-25 on angiogenesis, vascular remodelling and expression of angiogenic factors, compared changes with those in a "classical" ovalbumin (OVA)-induced murine asthma model. IL-25 and OVA were intranasally instilled into the airways of BALB/c mice for up to 55 days. Airways vessels and angiogenic factors, including Von Willebrand Factor (vWF), amphiregulin, angiogenin, endothelin-1, transcription factor ERG, basic fibroblast growth factor (bFGF), epidermal growth factor (EGF), insulin-like growth factor (IGF-1) and vascular endothelial growth factor (VEGF) in lung sections, homogenates and BAL fluid were detected and quantified by immunostaining or enzyme linked immunosorbent assay (ELISA). An in house assay was also utilised to compare the effects of IL-25 and other Th2-cytokines on angiogenesis by human vascular endothelial cells.

resultsRepetitive intranasal challenge with IL-25 alone or OVA alone in OVA-presensitised animals significantly increased peribronchial vWF (+) vessels in the murine airways, which was associated with remarkably elevated expression of amphiregulin, angiogenin, endothelin-1, bFGF, EGF, IGF-1, VEGF and ERG. IL-25, but not Th-2-cytokines induced human angiogenesis in vitro.

conclusionsThe data suggest that chronic exposure of murine airways to IL-25 alone is able to reproduce a local angiogenic milieu. Thus, blocking IL-25 may attenuate vascular remodelling and improve outcomes in asthma patients.

Indexed as

InterleukinsNeovascularization, PathologicVascular RemodelingAngiogenic ProteinsAnimalsAsthmaBronchoalveolar Lavage FluidCells, CulturedChronic DiseaseDisease Models, AnimalEndothelial CellsFemaleLungMice, Inbred BALB COvalbuminRecombinant ProteinsAngiogenic ProteinsInterleukinsMydgf protein, mouseOvalbuminRecombinant Proteins

Identifiers

PMID25889697
PMCPMC4390095
OpenAlexW2145159953

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.