Evidence map›Paper›PMID 29473905›Full record

ArticleInternational journal of molecular sciences2018

The In Vitro Effects of Enzymatic Digested Gliadin on the Functionality of the Autophagy Process.

Federico Manai, Alberto Azzalin, Fabio Gabriele, Carolina Martinelli, Martina Morandi, Marco Biggiogera, Mauro Bozzola, Sergio Comincini

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.3field-weighted citation impact, top 23% 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

13 citing papers in PubMed, 23 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Peculiar CaInternational journal of molecular sciences · 2023
    Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. MAGI2 Gene Region and Celiac Disease.Frontiers in nutrition · 2019
    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

8 authors at 1 institution in 1 country.

Federico ManaiDepartment of Biology and Biotechnology, University of Pavia, 27100 Pavia, Italy. federico.manai01@universitadipavia.it.
Alberto AzzalinDepartment of Biology and Biotechnology, University of Pavia, 27100 Pavia, Italy. azzalin.alberto@gmail.com.ORCID 0000-0001-6037-853X
Fabio GabrieleDepartment of Biology and Biotechnology, University of Pavia, 27100 Pavia, Italy. fabio.gabriele01@universitadipavia.it.
Carolina MartinelliDepartment of Biology and Biotechnology, University of Pavia, 27100 Pavia, Italy. carolina.martinelli991@gmail.com.
Martina MorandiDepartment of Biology and Biotechnology, University of Pavia, 27100 Pavia, Italy. martina.morandi01@universitadipavia.it.
Marco BiggiogeraDepartment of Biology and Biotechnology, University of Pavia, 27100 Pavia, Italy. marco.biggiogera@unipv.it.ORCID 0000-0003-3834-6712
Mauro BozzolaPediatrics and Adolescentology Unit, Department of Internal Medicine and Therapeutics, University of Pavia, Fondazione IRCCS San Matteo, 27100 Pavia, Italy. mauro.bozzola@unipv.it.ORCID 0000-0002-4882-3714
Sergio CominciniDepartment of Biology and Biotechnology, University of Pavia, 27100 Pavia, Italy. sergio.comincini@unipv.it.
University of Pavia · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gliadin, the alcohol-soluble protein fraction of wheat, contains the factor toxic for celiac disease (CD), and its toxicity is not reduced by digestion with gastro-pancreatic enzymes. Importantly, it is proved that an innate immunity to gliadin plays a key role in the development of CD. The immune response induces epithelial stress and reprograms intraepithelial lymphocytes into natural killer (NK)-like cells, leading to enterocyte apoptosis and an increase in epithelium permeability. In this contribution, we have reported that in Caco-2 cells the administration of enzymatically digested gliadin (PT-gliadin) reduced significantly the expression of the autophagy-related marker LC3-II. Furthermore, electron and fluorescent microscope analysis suggested a compromised functionality of the autophagosome apparatus. The rescue of the dysregulated autophagy process, along with a reduction of PT-gliadin toxicity, was obtained with a starvation induction protocol and by 3-methyladenine administration, while rapamycin, a well-known autophagy inducer, did not produce a significant improvement in the clearance of extra- and intra-cellular fluorescent PT-gliadin amount. Altogether, our results highlighted the possible contribution of the autophagy process in the degradation and in the reduction of extra-cellular release of gliadin peptides and suggest novel molecular targets to counteract gliadin-induced toxicity in CD.

Indexed as

ApoptosisAutophagyCaco-2 CellsCell SurvivalEndocytosisFluorescenceGliadinHumansMicrotubule-Associated ProteinsPepsin AProtein AggregatesTrypsinGliadinMAP1LC3A protein, humanMicrotubule-Associated ProteinsPepsin AProtein AggregatesTrypsinautophagosomeCaco-2 cellsceliac diseasegluten

Identifiers

PMID29473905
PMCPMC5855857
OpenAlexW2791238620

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.