Evidence map›Paper›PMID 34789272›Full record

ArticleJournal of neuroinflammation2021

Altered expression of fragile X mental retardation-1 (FMR1) in the thymus in autoimmune myasthenia gravis.

Scott Thomas, Odessa-Maud Fayet, Frédérique Truffault, Elie Fadel, Bastien Provost, Abderaouf Hamza, Sonia Berrih-Aknin, Jean-Paul Bonnefont, Rozen Le Panse

Open access · goldAbstract read
In one paragraph

Article in Journal of neuroinflammation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.2field-weighted citation impact, top 38% 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

3 citing papers in PubMed, 2 citations in OpenAlex.

  1. Review
  2. Review
  3. The role of mGenes & diseases · 2024
    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

9 authors at 3 institutions in 1 country.

Scott Thomas *Sorbonne University, INSERM, Institute of Myology, Center of Research in Myology, F-75013, Paris, France.
Odessa-Maud Fayet *Sorbonne University, INSERM, Institute of Myology, Center of Research in Myology, F-75013, Paris, France.
Frédérique TruffaultSorbonne University, INSERM, Institute of Myology, Center of Research in Myology, F-75013, Paris, France.
Elie FadelMarie Lannelongue Hospital, Paris-Sud University, Le Plessis-Robinson, France.
Bastien ProvostMarie Lannelongue Hospital, Paris-Sud University, Le Plessis-Robinson, France.
Abderaouf HamzaUniversité de Paris, Institut Imagine UMR1163, Hôpital Universitaire Necker-Enfants Malades, AP-HP, Paris, France.
Sonia Berrih-AkninSorbonne University, INSERM, Institute of Myology, Center of Research in Myology, F-75013, Paris, France.
Jean-Paul BonnefontUniversité de Paris, Institut Imagine UMR1163, Hôpital Universitaire Necker-Enfants Malades, AP-HP, Paris, France.
Rozen Le PanseSorbonne University, INSERM, Institute of Myology, Center of Research in Myology, F-75013, Paris, France. rozen.lepanse@upmc.fr.ORCID http://orcid.org/0000-0001-7522-5974
Inserm · FRHôpital Necker-Enfants Malades · FRUniversité Paris-Sud · FR

Funding

European Community FIGHT-MG/HEALTH-2009-242-210
6 · The paper itself

Abstract

Predisposition to autoimmunity and inflammatory disorders is observed in patients with fragile X-associated syndromes. These patients have increased numbers of CGG triplets in the 5' UTR region of FMR1 (Fragile X Mental Retardation 1) gene, that affects its expression. FMR1 is decreased in the thymus of myasthenia gravis (MG) patients, a prototypical autoimmune disease. We thus analyzed the number of CGG triplets in FMR1 in MG, and explored the regulatory mechanisms affecting thymic FMR1 expression. We measured the number of CGGs using thymic DNA from MG and controls, but no abnormalities in CGGs were found in MG that could explain thymic decrease of FMR1. We next analyzed by RT-PCR the expression of FMR1 and its transcription factors in thymic samples, and in thymic epithelial cell cultures in response to inflammatory stimuli. In control thymuses, FMR1 expression was higher in males than females, and correlated with CTCF (CCCTC-binding factor) expression. In MG thymuses, decreased expression of FMR1 was correlated with both CTCF and MAX (Myc-associated factor X) expression. Changes in FMR1 expression were supported by western blot analyses for FMRP. In addition, we demonstrated that FMR1, CTCF and MAX expression in thymic epithelial cells was also sensitive to inflammatory signals. Our results suggest that FMR1 could play a central role in the thymus and autoimmunity. First, in relation with the higher susceptibility of females to autoimmune diseases. Second, due to the modulation of its expression by inflammatory signals that are known to be altered in MG thymuses.

Indexed as

AdolescentAdultAutoimmunityCCCTC-Binding FactorCells, CulturedDNAEpithelial CellsFemaleFragile X Messenger Ribonucleoprotein 1HumansMaleMiddle AgedMyasthenia GravisSex CharacteristicsThymus GlandYoung AdultCCCTC-Binding FactorCTCF protein, humanDNAFMR1 protein, humanFragile X Messenger Ribonucleoprotein 1AutoimmunityCTCFFMR1Fragile X syndromesInflammatory cytokinesMaxMyasthenia gravisThymic epithelial cellsThymus

Identifiers

PMID34789272
PMCPMC8597299
OpenAlexW3213558030

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.