Evidence map›Paper›PMID 24835503›Full record

Trial reportThe Journal of allergy and clinical immunology2014

TGF-β1-induced phospholamban expression alters esophageal smooth muscle cell contraction in patients with eosinophilic esophagitis.

Lisa Y Beppu, Arjun A Anilkumar, Robert O Newbury, Ranjan Dohil, David H Broide, Seema S Aceves

Open access · greenAbstract readRandomized Controlled Trial
PubMed Full text at PMC Publisher
In one paragraph

Trial report in The Journal of allergy and clinical immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
7.9field-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

50 citing papers in PubMed, 71 citations in OpenAlex.

  1. Trial
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  7. Review
  8. Review
  9. Article
  10. Genetic and Molecular Contributors in Eosinophilic Esophagitis.Current allergy and asthma reports · 2023
    Review
  11. Breaking down the complex pathophysiology of eosinophilic esophagitis.Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology · 2023
    Review
  12. Article
  13. Article
  14. 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

6 authors at 1 institution in 1 country.

Lisa Y BeppuDivision of Allergy and Immunology, University of California, San Diego, Calif; Department of Pediatrics, University of California, San Diego, Calif.
Arjun A AnilkumarDivision of Allergy and Immunology, University of California, San Diego, Calif; Department of Medicine, University of California, San Diego, Calif.
Robert O NewburyDepartment of Pediatrics, University of California, San Diego, Calif; Division of Pathology, University of California, San Diego, Calif.
Ranjan DohilDepartment of Pediatrics, University of California, San Diego, Calif; Division of Gastroenterology, University of California, San Diego, Calif.
David H BroideDivision of Allergy and Immunology, University of California, San Diego, Calif; Department of Medicine, University of California, San Diego, Calif.
Seema S AcevesDivision of Allergy and Immunology, University of California, San Diego, Calif; Department of Pediatrics, University of California, San Diego, Calif; Department of Medicine, University of California, San Diego, Calif. Electronic address: saceves@ucsd.edu.
University of California, San Diego · US

Funding

TRM and airway inflammation and remodelingU19AI070535 · NIAID · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI BROIDE, DAVID H · 2006 to 2025
$34.2M
Chromosome 17q, allergic inflammation, and remodelingR01AI107779 · NIAID · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI BROIDE, DAVID H · 2013 to 2024
$4.7M
Mechanisms of tissue damage leading to chronic allergic eosinophilic esophagitisR01AI092135 · NIAID · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI ACEVES, SEEMA S · 2011 to 2020
$4.4M
Eosinophil trafficking and chronic tissue damage induced by allergic inflammationR37AI038425 · NIAID · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI BROIDE, DAVID H · 2007 to 2016
$3.7M
Siglec-F and Resolution of Allergic InflammationR01AI072115 · NIAID · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI BROIDE, DAVID H · 2008 to 2012
$1.7M
Contribution of rigid matrix to allergic eosinophilic esophagitis pathogenesisR56AI092135 · NIAID · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI ACEVES, SEEMA S · 2023 to 2023
$198k
NCATS NIH HHS UL1TR0001000NIAID NIH HHS AI 092135NIAID NIH HHS AI 107779NIAID NIH HHS AI 70535NIAID NIH HHS AI 72115NIAID NIH HHS R01 AI072115NIAID NIH HHS R01 AI092135NIAID NIH HHS R01 AI107779NIAID NIH HHS R37 AI038425NIAID NIH HHS R56 AI092135NIAID NIH HHS U19 AI070535
6 · The paper itself

Abstract

backgroundEosinophilic esophagitis (EoE) is a chronic antigen-mediated disease characterized by esophageal eosinophilia, remodeling, and fibrosis. TGF-β1 is a central regulator of EoE remodeling and increases esophageal smooth muscle (ESM) cell contraction.

objectiveIn this study we aimed to understand the molecular mechanisms by which TGF-β1 could induce ESM cell contraction.

methodsWe used primary human ESM cells and esophageal myofibroblasts (EMFs) to assess the mechanisms of TGF-β1-induced contraction. We analyzed the expression, phosphorylation, and function of phospholamban (PLN), a sarcoendoplasmic reticulum regulatory protein induced by TGF-β1. Expression of PLN, phospho-PLN, and its regulatory pathway was analyzed in the ESM of biopsy specimens from patients with EoE and control subjects. Gene silencing in EMFs from patients with EoE was used to understand the role of PLN in contraction.

resultsTGF-β1 induced and phosphorylated PLN in primary human ESM cells and EMFs from patients with EoE. PLN and phospho-PLN levels were increased in smooth muscle from patients with EoE compared with that seen in smooth muscle from control subjects in vivo. PLN inhibition significantly diminished TGF-β1-induced EMF contraction in patients with EoE. PLN expression and ESM/EMF contraction depended on TGF-β receptor I signals.

conclusionWe describe a previously unrecognized mechanism for ESM cell contraction that depends on TGF-β1, its receptors, and PLN. Because PLN levels are increased in smooth muscle from patients with EoE and PLN silencing diminishes contraction, we provide a novel potential mechanistic framework and therapeutic target for ESM dysfunction in patients with EoE.

Indexed as

Muscle ContractionAdultCalcium-Binding ProteinsCells, CulturedEosinophilic EsophagitisEsophagusFemaleGene Expression RegulationHumansMaleMuscle ProteinsMyocytes, Smooth MusclePhospholambanPhosphorylationTransforming Growth Factor beta1Calcium-Binding ProteinsMuscle ProteinsPhospholambanTGFB1 protein, humanTransforming Growth Factor beta1eosinophilsesophagusphospholambanRemodelingsmooth muscleTGF-β

Identifiers

PMID24835503
PMCPMC4231011
OpenAlexW2001490596

What OpenQuestion holds

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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.