Evidence map›Paper›PMID 20110557›Full record

ArticleAmerican journal of respiratory and critical care medicine2010

Decreased fibronectin production significantly contributes to dysregulated repair of asthmatic epithelium.

Anthony Kicic, Teal S Hallstrand, Erika N Sutanto, Paul T Stevens, Michael S Kobor, Christopher Taplin, Peter D Paré, Richard P Beyer, Stephen M Stick, Darryl A Knight

Abstract read
In one paragraph

Article in American journal of respiratory and critical care medicine, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed, 2 pooled it
8.0field-weighted citation impact, top 2% 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

74 citing papers in PubMed, 2 syntheses or guidelines pooled it, 158 citations in OpenAlex.

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14 more citing papers are in PubMed but not listed here.

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

10 authors at 4 institutions in 3 countries.

Anthony KicicDepartment of Respiratory Medicine, Princess Margaret Hospital for Children, Perth, 6001, Western Australia, Australia. anthonyk@ichr.uwa.edu.au
Teal S Hallstrand
Erika N Sutanto
Paul T Stevens
Michael S Kobor
Christopher Taplin
Peter D Paré
Richard P Beyer
Stephen M Stick
Darryl A Knight
The Kids Research Institute Australia · AUInstitute on Governance · CAPulmonary and Critical Care Associates · USUniversity of Washington · US

Funding

XENOBIOTIC BIOTRANSFORMATION AND DISPOSITIONP30ES007033 · NIEHS · UNIVERSITY OF WASHINGTON · PI Sheela Sathyanarayana · 1995 to 2026
$42.5M
Canadian Institutes of Health Research MOP-82745NIEHS NIH HHS P30ES07033
6 · The paper itself

Abstract

rationaleDamage to airway epithelium is followed by deposition of extracellular matrix (ECM) and migration of adjacent epithelial cells. We have shown that epithelial cells from children with asthma fail to heal a wound in vitro.

objectivesTo determine whether dysregulated ECM production by the epithelium plays a role in aberrant repair in asthma.

methodsAirway epithelial cells (AEC) from children with asthma (n = 36), healthy atopic control subjects (n = 23), and healthy nonatopic control subjects (n = 53) were investigated by microarray, gene expression and silencing, transcript regulation analysis, and ability to close mechanical wounds. MEASUREMENTS AND MAIN

resultsTime to repair a mechanical wound in vitro by AEC from healthy and atopic children was not significantly different and both were faster than AEC from children with asthma. Microarray analysis revealed differential expression of multiple gene sets associated with repair and remodeling in asthmatic AEC. Fibronectin (FN) was the only ECM component whose expression was significantly lower in asthmatic AEC. Expression differences were verified by quantitative polymerase chain reaction and ELISA, and reduced FN expression persisted in asthmatic cells over passage. Silencing of FN expression in nonasthmatic AEC inhibited wound repair, whereas addition of FN to asthmatic AEC restored reparative capacity. Asthmatic AEC failed to synthesize FN in response to wounding or cytokine/growth factor stimulation. Exposure to 5', 2'deoxyazacytidine had no effect on FN expression and subsequent analysis of the FN promoter did not show evidence of DNA methylation.

conclusionsThese data show that the reduced capacity of asthmatic epithelial cells to secrete FN is an important contributor to the dysregulated AEC repair observed in these cells.

Indexed as

AdolescentAsthmaAzacitidineCells, CulturedChildChild, PreschoolCycloheximideDexamethasoneDNA MethylationEnzyme-Linked Immunosorbent AssayEpithelial CellsExtracellular MatrixFibronectinsHomocystineHumansHydroxamic AcidsAzacitidineCycloheximideDexamethasoneFibronectinsHomocystineHydroxamic AcidsTetradecanoylphorbol AcetateTransforming Growth Factor beta1trichostatin A

Identifiers

PMID20110557
PMCPMC2862303
OpenAlexW2164891013

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.