ArticlePloS one2013
A celiac cellular phenotype, with altered LPP sub-cellular distribution, is inducible in controls by the toxic gliadin peptide P31-43.
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 17 papers, 2 of them syntheses that pooled it.
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Who cites it
17 citing papers in PubMed, 2 syntheses or guidelines pooled it, 26 citations in OpenAlex.
- Genetic determinants of skin ageing: a systematic review and meta-analysis of genome-wide association studies and candidate genes.Journal of physiological anthropology · 2025Pooled it
- 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
- Innate immune dysregulation in celiac disease and refractory celiac disease: mechanisms, management and emerging therapies.Frontiers in immunology · 2026Review
- Celiac Disease-Narrative Review on Progress in Celiac Disease.Foods (Basel, Switzerland) · 2025Review
- Advances in understanding and managing celiac disease: Pathophysiology and treatment strategies.World journal of gastroenterology · 2024Article
- Association ofGenes · 2024Article
- Article
- Pivotal Role of Inflammation in Celiac Disease.International journal of molecular sciences · 2022Review
- 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
- p31-43 Gliadin Peptide Forms Oligomers and Induces NLRP3 Inflammasome/Caspase 1- Dependent Mucosal Damage in Small Intestine.Frontiers in immunology · 2019Article
- Constitutive alterations in vesicular trafficking increase the sensitivity of cells from celiac disease patients to gliadin.Communications biology · 2019Article
- Anti-type 2 transglutaminase antibodies as modulators of type 2 transglutaminase functions: a possible pathological role in celiac disease.Cellular and molecular life sciences : CMLS · 2018Review
- Differences of immune disorders between Alzheimer's disease and breast cancer based on transcriptional regulation.PloS one · 2017Article
- Gliadin peptides as triggers of the proliferative and stress/innate immune response of the celiac small intestinal mucosa.International journal of molecular sciences · 2014Review
Corrections and comments
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Celiac disease (CD) is a frequent inflammatory intestinal disease, with a genetic background, caused by gliadin-containing food. Undigested gliadin peptides P31-43 and P57-68 induce innate and adaptive T cell-mediated immune responses, respectively. Alterations in the cell shape and actin cytoskeleton are present in celiac enterocytes, and gliadin peptides induce actin rearrangements in both the CD mucosa and cell lines. Cell shape is maintained by the actin cytoskeleton and focal adhesions, sites of membrane attachment to the extracellular matrix. The locus of the human Lipoma Preferred Partner (LPP) gene was identified as strongly associated with CD using genome-wide association studies (GWAS). The LPP protein plays an important role in focal adhesion architecture and acts as a transcription factor in the nucleus. In this study, we examined the hypothesis that a constitutive alteration of the cell shape and the cytoskeleton, involving LPP, occurs in a cell compartment far from the main inflammation site in CD fibroblasts from skin explants. We analyzed the cell shape, actin organization, focal adhesion number, focal adhesion proteins, LPP sub-cellular distribution and adhesion to fibronectin of fibroblasts obtained from CD patients on a Gluten-Free Diet (GFD) and controls, without and with treatment with A-gliadin peptide P31-43. We observed a "CD cellular phenotype" in these fibroblasts, characterized by an altered cell shape and actin organization, increased number of focal adhesions, and altered intracellular LPP protein distribution. The treatment of controls fibroblasts with gliadin peptide P31-43 mimics the CD cellular phenotype regarding the cell shape, adhesion capacity, focal adhesion number and LPP sub-cellular distribution, suggesting a close association between these alterations and CD pathogenesis.
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