Evidence map›Paper›PMID 15223860›Full record

ArticleThorax2004

Epithelial expression and release of FGF-2 from heparan sulphate binding sites in bronchial tissue in asthma.

J K Shute, N Solic, J Shimizu, W McConnell, A E Redington, P H Howarth

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Thorax, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.4field-weighted citation impact, top 21% 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, 59 citations in OpenAlex.

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  17. IL-9 governs allergen-induced mast cell numbers in the lung and chronic remodeling of the airways.American journal of respiratory and critical care medicine · 2011
    Article
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  19. Review
  20. Respiratory syncytial virus infection provokes airway remodelling in allergen-exposed mice in absence of prior allergen sensitization.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2008
    Article
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

6 authors at 1 institution in 1 country.

J K ShuteDepartment of Medical Specialties, Southampton General Hospital, Southampton SO16 6YD, UK. jan.shute@port.ac.uk
N Solic
J Shimizu
W McConnell
A E Redington
P H Howarth
University of Portsmouth · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe most characteristic structural change evident in endobronchial biopsies in asthma, even in mild disease, is subepithelial collagen deposition within the lamina reticularis. This has been associated with progressive loss of lung function and the persistence of airway hyperresponsiveness, and has been linked to airway fibroblast proliferation. A potent fibroproliferative factor in bronchoalveolar lavage fluid in asthma is fibroblast growth factor-2 (FGF-2). FGF-2 is a member of a family of heparin binding growth factors that bind to heparan sulphate proteoglycans (HSPG), an important determinant of FGF-2 activity. This study compared the level of expression and distribution of FGF-2 in relation to HSPG in bronchial tissue from normal and asthmatic subjects.

methodsThe distribution of FGF-2 and HSPG in intact and cleaved forms in endobronchial biopsies from normal and asthmatic subjects was examined using an immunohistochemical approach. A novel ELISA based method was developed to detect solubilisation of FGF-2 following addition of heparin and heparitinase to bronchial tissue slices.

resultsImmunohistochemical analysis showed that FGF-2 was co-localised to HSPG in epithelial and endothelial basement membranes. Epithelial FGF-2, but not HSPG, was significantly more abundant in patients with mild asthma than in normal subjects. In vitro experiments indicated that FGF-2 was released from binding sites in the tissue by heparin and heparitinase I.

conclusionsFGF-2 is bound by HSPG in bronchial tissue. The mast cell, through the release of heparin and endoglycosidase, may make a unique contribution to tissue remodelling in allergic asthma.

Indexed as

AdultAsthmaBinding SitesBronchiBronchoalveolar Lavage FluidEpithelial CellsFemaleFibroblast Growth Factor 2Forced Expiratory VolumeHeparan Sulfate ProteoglycansHeparin LyaseHumansImmunohistochemistryMaleMatrix Metalloproteinase 3StreptokinaseFibroblast Growth Factor 2Heparan Sulfate ProteoglycansHeparin LyaseMatrix Metalloproteinase 3Streptokinase

Identifiers

PMID15223860
PMCPMC1747073
OpenAlexW2160053403

What OpenQuestion holds

Textmetadata
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.