ArticlePloS one2013
Enterocyte proliferation and signaling are constitutively altered in celiac disease.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.
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Who cites it
20 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.
- Association of LPP and TAGAP Polymorphisms with Celiac Disease Risk: A Meta-Analysis.International journal of environmental research and public health · 2017Pooled it
- Pediatric Celiac Disease Patients Show Alterations of Dendritic Cell Shape and Actin Rearrangement.International journal of molecular sciences · 2021Trial
- Proteomic Analysis Highlights Peculiar Protein and Phosphoprotein Profiles in Dermal Fibroblasts from Celiac Disease Patients.International journal of molecular sciences · 2026Article
- Review
- Overview of the compromised mucosal integrity in celiac disease.Journal of molecular histology · 2024Review
- Review
- Peculiar CaInternational journal of molecular sciences · 2023Article
- Article
- Mucosal Healing in Celiac Disease: Villous Architecture and Immunohistochemical Features in Children on a Long-Term Gluten Free Diet.Nutrients · 2022Article
- Type 2 Transglutaminase in Coeliac Disease: A Key Player in Pathogenesis, Diagnosis and Therapy.International journal of molecular sciences · 2022Review
- Pivotal Role of Inflammation in Celiac Disease.International journal of molecular sciences · 2022Review
- Expression of Selected Genes and Circulating microRNAs in Patients with Celiac Disease.Medicina (Kaunas, Lithuania) · 2022Article
- Interplay between Type 2 Transglutaminase (TG2), Gliadin Peptide 31-43 and Anti-TG2 Antibodies in Celiac Disease.International journal of molecular sciences · 2020Review
- Constitutive Differential Features of Type 2 Transglutaminase in Cells Derived from Celiac Patients and from Healthy Subjects.International journal of molecular sciences · 2020Article
- Effects ofFrontiers in immunology · 2020Article
- Constitutive alterations in vesicular trafficking increase the sensitivity of cells from celiac disease patients to gliadin.Communications biology · 2019Article
- The Transcriptomic Analysis of Circulating Immune Cells in a Celiac Family Unveils Further Insights Into Disease Pathogenesis.Frontiers in medicine · 2018Article
- Immunopathogenesis and therapeutic approaches in pediatric celiac disease.Expert review of clinical immunology · 2016Review
- Gliadin peptides as triggers of the proliferative and stress/innate immune response of the celiac small intestinal mucosa.International journal of molecular sciences · 2014Review
- A celiac cellular phenotype, with altered LPP sub-cellular distribution, is inducible in controls by the toxic gliadin peptide P31-43.PloS one · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Celiac disease (CD) occurs frequently, and is caused by ingestion of prolamins from cereals in subjects with a genetic predisposition. The small intestinal damage depends on an intestinal stress/innate immune response to certain gliadin peptides (e.g., A-gliadin P31-43) in association with an adaptive immune response to other gliadin peptides (e.g., A-gliadin P57-68). Gliadin and peptide P31-43 affect epithelial growth factor receptor (EGFR) signaling and CD enterocyte proliferation. The reason why the stress/innate immune and proliferative responses to certain gliadin peptides are present in CD and not in control intestine is so far unknown. The aim of this work is to investigate if, in CD, a constitutive alteration of enterocyte proliferation and signaling exists that may represent a predisposing condition to the damaging effects of gliadin. Immunofluorescence and immunohistochemistry were used to study signaling in CD fibroblasts and intestinal biopsies. Western blot (WB) analysis, immunoprecipitation, and quantitative PCR were also used. We found in CD enterocytes enhancement of both proliferation and Epidermal Growth Factor Receptor (EGFR)/ligand system. In CD enterocytes and fibroblasts we found increase of the phosphorylated downstream signaling molecule Extracellular Signal Regulated Kinase (ERK); block of the ERK activation normalizes enterocytes proliferation in CD mucosa. In conclusion the same pathway, which gliadin and gliadin peptide P31-43 can interfere with, is constitutively altered in CD cells. This observation potentially explains the specificity of the damaging effects of certain gliadin peptides on CD intestine.
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Registered trials
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.