Evidence map›Paper›PMID 24138138›Full record

ArticleRespiratory research2013

Airway hyperresponsiveness is associated with airway remodeling but not inflammation in aging Cav1-/- mice.

Kelsa E Gabehart, Simon G Royce, Diego J Maselli, Shelley K Miyasato, Elaine C Davis, Mimi L K Tang, Claude Jourdan Le Saux

Open access · goldAbstract readComparative Study
In one paragraph

Article in Respiratory research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

18 citing papers in PubMed, 31 citations in OpenAlex.

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  7. The STAT6 inhibitor AS1517499 reduces the risk of asthma in mice with 2,4-dinitrochlorobenzene-induced atopic dermatitis by blocking the STAT6 signaling pathway.Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology · 2022
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  12. Paucigranulocytic asthma: Uncoupling of airway obstruction from inflammation.The Journal of allergy and clinical immunology · 2019
    Review
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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

7 authors at 4 institutions in 3 countries.

Kelsa E Gabehart
Simon G Royce
Diego J Maselli
Shelley K Miyasato
Elaine C Davis
Mimi L K Tang
Claude Jourdan Le SauxDepartment of Cell and Molecular Biology, John A, Burns School of Medicine, University of Hawaii, Honolulu, HI, USA. lesaux@uthscsa.edu.
Murdoch Children's Research Institute · AUThe University of Texas Health Science Center at San Antonio · USUniversity of Hawaiʻi at Mānoa · USMcGill University · CA

Funding

USING EEG COMPLEXITY AND HIGH PERFORMANCE COMPUTING TO PROFILE SLEEPP20RR016467 · NCRR · UNIVERSITY OF HAWAII AT MANOA · PI HOLMES, ERIC · 2001 to 2011
$24.5M
NCRR NIH HHS P20RR016467
6 · The paper itself

Abstract

backgroundAirway inflammation and airway remodeling are the key contributors to airway hyperresponsiveness (AHR), a characteristic feature of asthma. Both processes are regulated by Transforming Growth Factor (TGF)-β. Caveolin 1 (Cav1) is a membrane bound protein that binds to a variety of receptor and signaling proteins, including the TGF-β receptors. We hypothesized that caveolin-1 deficiency promotes structural alterations of the airways that develop with age will predispose to an increased response to allergen challenge.

methodsAHR was measured in Cav1-deficient and wild-type (WT) mice 1 to 12 months of age to examine the role of Cav1 in AHR and the relative contribution of inflammation and airway remodeling. AHR was then measured in Cav1-/- and WT mice after an ovalbumin-allergen challenge performed at either 2 months of age, when remodeling in Cav1-/- and WT mice was equivalent, and at 6 months of age, when the Cav1-/- mice had established airway remodeling.

resultsCav1-/- mice developed increased thickness of the subepithelial layer and a correspondingly increased AHR as they aged. In addition, allergen-challenged Cav1-/- mice had an increase in AHR greater than WT mice that was largely independent of inflammation. Cav1-/- mice challenged at 6 months of age have decreased AHR compared to those challenged at 2 months with correspondingly decreased BAL IL-4 and IL-5 levels, inflammatory cell counts and percentage of eosinophils. In addition, in response to OVA challenge, the number of goblet cells and α-SMA positive cells in the airways were reduced with age in response to OVA challenge in contrast to an increased collagen deposition further enhanced in absence of Cav1.

conclusionA lack of Cav1 contributed to the thickness of the subepithelial layer in mice as they aged resulting in an increase in AHR independent of inflammation, demonstrating the important contribution of airway structural changes to AHR. In addition, age in the Cav1-/- mice is a contributing factor to airway remodeling in the response to allergen challenge.

Indexed as

ActinsAgingAirway RemodelingAnimalsAsthmaBronchial HyperreactivityCaveolin 1CollagenDisease Models, AnimalFemaleInterleukin-4Interleukin-5MiceMice, Inbred C57BLMice, KnockoutOvalbuminActinsCaveolin 1CollagenInterleukin-4Interleukin-5OvalbuminTransforming Growth Factor beta

Identifiers

PMID24138138
PMCPMC4015038
OpenAlexW2169043559

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.