Evidence map›Paper›PMID 24499258›Full record

ArticleAllergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology2013

IgE induces proliferation in human airway smooth muscle cells: role of MAPK and STAT3 pathways.

Naresh Singh Redhu, Lianyu Shan, Duaa Al-Subait, Heather L Ashdown, Hesam Movassagh, Bouchaib Lamkhioued, Abdelilah S Gounni

Open access · goldAbstract read
In one paragraph

Article in Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

19 citing papers in PubMed, 44 citations in OpenAlex.

  1. Trial
  2. LAPTM5 potentiates airway remodeling by regulating MAPKs-mediated airway smooth muscle cells' dysfunction.Mammalian genome : official journal of the International Mammalian Genome Society · 2026
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  6. Development of Adaptive Immunity and Its Role in Lung Remodeling.Advances in experimental medicine and biology · 2023
    Article
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  17. The impact of vitamin D on asthmatic human airway smooth muscle.Expert review of respiratory medicine · 2016
    Article
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  19. 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

7 authors at 2 institutions in 3 countries.

Naresh Singh Redhu
Lianyu Shan
Duaa Al-Subait
Heather L Ashdown
Hesam Movassagh
Bouchaib Lamkhioued
Abdelilah S GounniDepartment of Immunology, Faculty of Medicine, University of Manitoba, 419 Apotex Centre- 750 McDermot Ave, Winnipeg, MB R3E 0T5, Canada. abdel.gounni@med.umanitoba.ca.
University of Manitoba · CAUniversité de Reims Champagne-Ardenne · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Airway remodeling is not specifically targeted by current asthma medications, partly owing to the lack of understanding of remodeling mechanisms, altogether posing great challenges in asthma treatment. Increased airway smooth muscle (ASM) mass due to hyperplasia/hypertrophy contributes significantly to overall airway remodeling and correlates with decline in lung function. Recent evidence suggests that IgE sensitization can enhance the survival and mediator release in inflammatory cells. Human ASM (HASM) cells express both low affinity (FcεRII/CD23) and high affinity IgE Fc receptors (FcεRI), and IgE can modulate the contractile and synthetic function of HASM cells. IgE was recently shown to induce HASM cell proliferation but the detailed mechanisms remain unknown. We report here that IgE sensitization induces HASM cell proliferation, as measured by 3H-thymidine, EdU incorporation, and manual cell counting. As an upstream signature component of FcεRI signaling, inhibition of spleen tyrosine kinase (Syk) abrogated the IgE-induced HASM proliferation. Further analysis of IgE-induced signaling depicted an IgE-mediated activation of Erk 1/2, p38, JNK MAPK, and Akt kinases. Lastly, lentiviral-shRNA-mediated STAT3 silencing completely abolished the IgE-mediated HASM cell proliferation. Collectively, our data provide mechanisms of a novel function of IgE which may contribute, at least in part, to airway remodeling observed in allergic asthma by directly inducing HASM cell proliferation.

Identifiers

PMID24499258
PMCPMC3842672
OpenAlexW2147230949

What OpenQuestion holds

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LicenceCC BY
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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.