Evidence map›Paper›PMID 25480337›Full record

ArticleAmerican journal of physiology. Lung cellular and molecular physiology2015

The cardiac protein αT-catenin contributes to chemical-induced asthma.

Stephen Sai Folmsbee, Luisa Morales-Nebreda, Jolanda Van Hengel, Koen Tyberghein, Frans Van Roy, G R Scott Budinger, Paul J Bryce, Cara J Gottardi

Abstract read
In one paragraph

Article in American journal of physiology. Lung cellular and molecular physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

12 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Loss of α(E)-catenin promotes Fas mediated apoptosis in tubular epithelial cells.Apoptosis : an international journal on programmed cell death · 2015
    Article
  11. Review
  12. 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

8 authors.

Stephen Sai FolmsbeeDepartment of Pulmonary and Critical Care Medicine, Northwestern University Feinberg School of Medicine, Chicago, Illinois; The Driskill Graduate Training Program in Life Sciences, Northwestern University Feinberg School of Medicine, Chicago, Illinois;
Luisa Morales-NebredaDepartment of Pulmonary and Critical Care Medicine, Northwestern University Feinberg School of Medicine, Chicago, Illinois;
Jolanda Van HengelDepartment of Basic Medical Sciences, Faculty of Medicine and Health Sciences, Ghent, Belgium; Department of Biomedical Molecular Biology, Molecular Cell Biology Unit, Ghent University, Ghent, Belgium; and Inflammation Research Center, Flanders Institute for Biotechnology (VIB), Ghent, Belgium.
Koen TybergheinDepartment of Biomedical Molecular Biology, Molecular Cell Biology Unit, Ghent University, Ghent, Belgium; and Inflammation Research Center, Flanders Institute for Biotechnology (VIB), Ghent, Belgium.
Frans Van RoyDepartment of Biomedical Molecular Biology, Molecular Cell Biology Unit, Ghent University, Ghent, Belgium; and Inflammation Research Center, Flanders Institute for Biotechnology (VIB), Ghent, Belgium.
G R Scott BudingerDepartment of Pulmonary and Critical Care Medicine, Northwestern University Feinberg School of Medicine, Chicago, Illinois;
Paul J BryceDepartment of Allergy and Immunology, Northwestern University Feinberg School of Medicine, Chicago, Illinois;
Cara J GottardiDepartment of Pulmonary and Critical Care Medicine, Northwestern University Feinberg School of Medicine, Chicago, Illinois; Department of Cellular and Molecular Biology, Northwestern University Feinberg School of Medicine, Chicago, Illinois; c-gottardi@northwestern.edu.

Funding

Tumor Environment and Metastasis (TEAM) Research ProgramP30CA060553 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI LEONIDAS C. PLATANIAS · 1993 to 2026
$153.9M
CARCINOGENESIS TRAINING PROGRAMT32CA009560 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI Kathleen Janee Green · 1986 to 2026
$8.4M
Signaling in the lung induced by particulate matter air pollutionR01ES013995 · NIEHS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI BUDINGER, GR SCOTT · 2006 to 2015
$3.3M
Mechanism of nuclear signaling and cell-cell adhesion by cateninsR01GM076561 · NIGMS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI GOTTARDI, CARA J · 2006 to 2015
$2.8M
Role for Wnt/beta-catenin signaling in alveolar repair and fibrosisR01HL094643 · NHLBI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI GOTTARDI, CARA J · 2011 to 2014
$1.5M
The role of alpha-T-catenin in the pathogenesis of occupational asthmaF30ES024622 · NIEHS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI FOLMSBEE, STEPHEN SAI · 2015 to 2017
$111k
The Role of Mitochondrial Reactive Oxygen Species in TGF-Beta SignalingI01BX000201 · VA · JESSE BROWN VA MEDICAL CENTER · PI BUDINGER, GR SCOTT, JAIN, MANU · 2011 to 2017
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BLRD VA I01 BX000201NCI NIH HHS P30 CA060553NCI NIH HHS T32 CA009560NCI NIH HHS T32CA09560NIEHS NIH HHS F30 ES024622NIEHS NIH HHS R01 ES013995NIGMS NIH HHS GM076561
6 · The paper itself

Abstract

Ten to 25% of adult asthma is occupational induced, a subtype caused by exposure to workplace chemicals. A recent genomewide association study identified single-nucleotide polymorphisms in the cardiac protein αT-catenin (αT-cat) that correlated with the incidence and severity of toluene diisocyanate (TDI) occupational asthma. αT-cat is a critical mediator of cell-cell adhesion and is predominantly expressed in cardiomyocytes, but its connection to asthma remains unknown. Therefore, we sought to determine the primary αT-cat-expressing cell type in the lung and its contribution to lung physiology in a murine model of TDI asthma. We show that αT-cat is expressed in lung within the cardiac sheath of pulmonary veins. Mechanically ventilated αT-cat knockout (KO) mice exhibit a significantly increased pressure-volume curve area compared with wild-type (WT) mice, suggesting that αT-cat loss affects lung hysteresis. Using a murine model of TDI asthma, we find that αT-cat KO mice show increased airway hyperresponsiveness to methacholine compared with WT mice. Bronchoalveolar lavage reveals only a mild macrophage-dominant inflammation that is not significantly different between WT and KO mice. These data suggest that αT-cat may contribute to asthma through a mechanism independent of inflammation and related to heart and pulmonary vein dysfunction.

Indexed as

Air Pollutantsalpha CateninAnimalsAsthma, OccupationalCells, CulturedFemaleHumansIntercellular JunctionsLungMice, Inbred C57BLMice, KnockoutMyocytes, CardiacPulmonary VeinsToluene 2,4-DiisocyanateAir Pollutantsalpha CateninCTNNA3 protein, mouseToluene 2,4-Diisocyanatecell-cell adhesionlung hysteresisoccupational asthmaαT-catenin

Identifiers

PMID25480337
PMCPMC4340121

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.