Evidence map›Paper›PMID 31660029›Full record

ArticleWorld journal of gastroenterology2019

Role of tristetraprolin phosphorylation in paediatric patients with inflammatory bowel disease.

Alessia Di Silvestre, Marianna Lucafò, Letizia Pugnetti, Matteo Bramuzzo, Gabriele Stocco, Egidio Barbi, Giuliana Decorti

Open access · hybridAbstract read
In one paragraph

Article in World journal of gastroenterology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.2field-weighted citation impact, top 47% 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

6 citing papers in PubMed, 5 citations in OpenAlex.

  1. Review
  2. The EGR1/ZFP36 axis governs glycosphingolipid metabolic reprogramming in monocyte-derived macrophages in guillain-barré syndrome.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026
    Article
  3. Post-transcriptional checkpoints in autoimmunity.Nature reviews. Rheumatology · 2023
    Review
  4. The Loss of YTHDC1 in Gut Macrophages Exacerbates Inflammatory Bowel Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023
    Article
  5. Review
  6. Review
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 4 institutions in 3 countries.

Alessia Di SilvestrePhD School in Science of Reproduction and Development, University of Trieste, Trieste 34127, Italy.
Marianna LucafòInstitute for Maternal and Child Health, IRCCS "Burlo Garofolo", Trieste 34137, Italy.
Letizia PugnettiPhD School in Science of Reproduction and Development, University of Trieste, Trieste 34127, Italy.
Matteo BramuzzoInstitute for Maternal and Child Health, IRCCS "Burlo Garofolo", Trieste 34137, Italy.
Gabriele StoccoDepartment of Life Sciences, University of Trieste, Trieste 34127, Italy.
Egidio BarbiInstitute for Maternal and Child Health, IRCCS "Burlo Garofolo", Trieste 34137, Italy.
Giuliana DecortiInstitute for Maternal and Child Health, IRCCS "Burlo Garofolo", Trieste 34137, Italy. decorti@units.it.
IRCCS Materno Infantile Burlo Garofolo · ITShowa University Fujigaoka Hospital · JPCreative Research Enterprises (United States) · USUniversity of Trieste · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIntestinal inflammation and epithelial injury are the leading actors of inflammatory bowel disease (IBD), causing an excessive pro-inflammatory cytokines expression. Tristetraprolin (TTP), an mRNA binding protein, plays a role in regulating the inflammatory factors, recognizing specific sequences on the 3' untranslated region of cytokine mRNAs. TTP activity depends on its phosphorylation state: the unphosphorylated TTP degrades pro-inflammatory cytokine mRNAs; on the contrary, the phosphorylated TTP fails to destabilize mRNAs furthering their expression. The phospho-TTP forms a complex with the chaperone protein 14-3-3. This binding could be one of the factors that promote intestinal inflammation as a cause of disease progression.

aimTo assess if TTP phosphorylation has a role in paediatric IBD.

methodsThe study was carried out on a cohort of paediatric IBD patients. For each patient enrolled, a specimen of inflamed and non-inflamed colonic mucosa was collected. Furthermore, the experiments were conducted on macrophages differentiated from blood samples of the same patients. Macrophages from healthy donors' blood were used as controls. Co-immunoprecipitation assay and immunoblotting analyses were performed to observe the formation of the phospho-TTP/14-3-3 complex. In the same samples TNF-α expression was also evaluated as major factor of the pro-inflammatory activity.

resultsIn this work we studied indirectly the phosphorylation of TTP through the binding with the chaperone protein 14-3-3. In inflamed and non-inflamed colon mucosa of IBD paediatric patients immunoblot assay demonstrated a higher expression of the TTP in inflamed samples respect to the non-inflamed; the co-immunoprecipitated 14-3-3 protein showed the same trend of expression. In the

conclusionIn this work, for the first time, we describe a relation between phospho-TTP/14-3-3 complex and IBD. Indeed, a higher expression of TTP/14-3-3 was recorded in IBD samples in comparison to controls.

Indexed as

14-3-3 ProteinsBiopsyChildCohort StudiesColitis, UlcerativeColonColonoscopyCrohn DiseaseHumansIntestinal MucosaMalePhosphorylationTristetraprolin14-3-3 ProteinsTristetraprolinZFP36 protein, human14-3-3 proteinCytokinesInflammationInflammatory bowel diseasePhosphorylationTristetraprolin

Identifiers

PMID31660029
PMCPMC6815796
OpenAlexW2980914196

What OpenQuestion holds

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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.