Evidence map›Paper›PMID 24987792›Full record

ArticleAmerican journal of respiratory cell and molecular biology2015

Cross-talk between human mast cells and bronchial epithelial cells in plasminogen activator inhibitor-1 production via transforming growth factor-β1.

Seong H Cho, Sun H Lee, Atsushi Kato, Tetsuji Takabayashi, Marianna Kulka, Soon C Shin, Robert P Schleimer

Open access · greenAbstract read
In one paragraph

Article in American journal of respiratory cell and molecular biology, 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
1.2field-weighted citation impact, top 22% 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, 27 citations in OpenAlex.

  1. Trial
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  7. Asthma and obesity: endotoxin another insult to add to injury?Clinical science (London, England : 1979) · 2021
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  8. Dermal Extracellular Matrix-Derived Hydrogels as anTissue engineering. Part A · 2021
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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 2 institutions in 3 countries.

Seong H Cho1 Division of Allergy-Immunology, Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, Illinois.
Sun H Lee
Atsushi Kato
Tetsuji Takabayashi
Marianna Kulka
Soon C Shin
Robert P Schleimer
Northwestern University · USNational Institute for Nanotechnology · CA

Funding

Systems Genetics Approach to Gene Discovery in Chronic RhinosinusitisU19AI106683 · NIAID · NORTHWESTERN UNIVERSITY AT CHICAGO · PI KERN, ROBERT C · 2014 to 2017
$7.9M
Glucocorticosteroid Action In Inflammatory DiseaseR37HL068546 · NHLBI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI SCHLEIMER, ROBERT P · 2009 to 2018
$3.5M
Role of Epithelium in Immunity, Inflammation and DiseaseR01HL078860 · NHLBI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI SCHLEIMER, ROBERT P · 2006 to 2013
$3.0M
Systems Genetics Approach to Gene Discovery in Chronic RhinosinusitisP01AI106683 · NIAID · NORTHWESTERN UNIVERSITY AT CHICAGO · PI OBER, CAROLE · 2013 to 2013
$1.7M
NHLBI NIH HHS R01 HL078860NHLBI NIH HHS R01HL078860NHLBI NIH HHS R37HL0546NHLBI NIH HHS R37 HL068546NIAID NIH HHS AI106683NIAID NIH HHS P01 AI106683NIAID NIH HHS U19 AI106683
6 · The paper itself

Abstract

Previous reports suggest that plasminogen activator inhibitor-1 (PAI-1) promotes airway remodeling and that human and mouse mast cells (MCs) are an important source of PAI-1. In the present study we investigated MC-epithelial cell (EC) interactions in the production of PAI-1. We stimulated the human MC line LAD2 with IgE-receptor cross-linking and collected the supernatants. We incubated the human bronchial EC line BEAS-2B with the LAD2 supernatants and measured the level of PAI-1. When the supernatants from IgE-stimulated LAD2 were added to BEAS-2B, there was a significant enhancement of PAI-1 production by BEAS-2B. When we treated the MC supernatants with a transforming growth factor (TGF)-β1 neutralizing antibody, the MC-derived induction of PAI-1 from BEAS-2B was completely abrogated. Although TGF-β1 mRNA was constitutively expressed in resting LAD2, it was not highly induced by IgE-mediated stimulation. Nonetheless, active TGF-β1 protein was significantly increased in LAD2 after IgE-mediated stimulation. Active TGF-β1 produced by primary cultured human MCs was significantly reduced in the presence of a chymase inhibitor, suggesting a role of MC chymase as an activator of latent TGF-β1. This study indicates that stimulation of human MCs by IgE receptor cross-linking triggers activation of TGF-β1, at least in part via chymase, which in turn induces the production of PAI-1 by bronchial ECs. Our data suggest that human MCs may play an important role in airway remodeling in asthma as a direct source of PAI-1 and by activating bronchial ECs to produce further PAI-1 via a TGF-β1-mediated activation pathway.

Indexed as

Cell CommunicationAnimalsAsthmaBronchiCell LineChymasesEpithelial CellsHumansImmunoglobulin EMast CellsMicePlasminogen Activator Inhibitor 1RNA, MessengerSerpin E2Transforming Growth Factor beta1ChymasesImmunoglobulin EPlasminogen Activator Inhibitor 1RNA, MessengerSERPINE1 protein, humanSerpin E2Serpine2 protein, mouseTGFB1 protein, humanTgfb1 protein, mouseTransforming Growth Factor beta1chymaseepithelial cellsmast cellsplasminogen activator inhibitor-1transforming growth factor-β1

Identifiers

PMID24987792
PMCPMC4370249
OpenAlexW2128308244

What OpenQuestion holds

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Read underepoch 390

Registered trials

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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.