Evidence map›Paper›PMID 37334284›Full record

ArticleFrontiers in endocrinology2023

NOD mouse dorsal root ganglia display morphological and gene expression defects before and during autoimmune diabetes development.

Marta Corral-Pujol, Berta Arpa, Estela Rosell-Mases, Leire Egia-Mendikute, Conchi Mora, Thomas Stratmann, Alex Sanchez, Anna Casanovas, Josep Enric Esquerda, Didac Mauricio and 2 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in endocrinology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
0.2field-weighted citation impact, top 49% 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

0 citing papers in PubMed, 1 citations in OpenAlex.

No citing paper in PubMed yet.

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

12 authors at 6 institutions in 1 country.

Marta Corral-PujolImmunology Unit, Department of Experimental Medicine, Faculty of Medicine, University of Lleida and IRBLleida, Lleida, Spain.
Berta ArpaImmunology Unit, Department of Experimental Medicine, Faculty of Medicine, University of Lleida and IRBLleida, Lleida, Spain.
Estela Rosell-MasesImmunology Unit, Department of Experimental Medicine, Faculty of Medicine, University of Lleida and IRBLleida, Lleida, Spain.
Leire Egia-MendikuteImmunology Unit, Department of Experimental Medicine, Faculty of Medicine, University of Lleida and IRBLleida, Lleida, Spain.
Conchi MoraImmunology Unit, Department of Experimental Medicine, Faculty of Medicine, University of Lleida and IRBLleida, Lleida, Spain.
Thomas StratmannDepartment of Cell Biology, Physiology and Immunology, Faculty of Biology, University of Barcelona, Barcelona, Spain.
Alex SanchezGenetics, Microbiology and Statistics Department, Universitat de Barcelona, Barcelona, Spain.
Anna CasanovasPatologia Neuromuscular Experimental Departament de Medicina Experimental, Facultat de Medicina, Universitat de Lleida and Institut de Recerca Biomèdica de Lleida (IRBLleida), Lleida, Spain.
Josep Enric EsquerdaPatologia Neuromuscular Experimental Departament de Medicina Experimental, Facultat de Medicina, Universitat de Lleida and Institut de Recerca Biomèdica de Lleida (IRBLleida), Lleida, Spain.
Didac MauricioDepartment of Endocrinology and Nutrition, Hospital de la Santa Creu i Sant Pau and Institut d'Investigació Biomèdica Sant Pau (IIB Sant Pau), Barcelona, Spain.
Marta Vives-PiImmunology Department, Germans Trias i Pujol Research Institute, Badalona, Spain.
Joan VerdaguerImmunology Unit, Department of Experimental Medicine, Faculty of Medicine, University of Lleida and IRBLleida, Lleida, Spain.
Universitat de Lleida · ESInstituto de Investigación Biomédica de Lleida · ESInstituto de Salud Carlos III · ESUniversitat Autònoma de Barcelona · ESUniversitat de Barcelona · ESVall d'Hebron Institut de Recerca · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: During the development of Autoimmune Diabetes (AD) an autoimmune attack against the Peripheral Nervous System occurs. To gain insight into this topic, analyses of Dorsal Root Ganglia (DRG) from Non-Obese Diabetic (NOD) mice were carried out. Methods: Histopathological analysis by electron and optical microscopy in DRG samples, and mRNA expression analyzes by the microarray technique in DRG and blood leukocyte samples from NOD and C57BL/6 mice were performed. Results: The results showed the formation of cytoplasmic vacuoles in DRG cells early in life that could be related to a neurodegenerative process. In view of these results, mRNA expression analyses were conducted to determine the cause and/or the molecules involved in this suspected disorder. The results showed that DRG cells from NOD mice have alterations in the transcription of a wide range of genes, which explain the previously observed alterations. In addition, differences in the transcription genes in white blood cells were also detected. Discussion: Taken together, these results indicate that functional defects are not only seen in beta cells but also in DRG in NOD mice. These results also indicate that these defects are not a consequence of the autoimmune process that takes place in NOD mice and suggest that they may be involved as triggers for its development.

Indexed as

Diabetes Mellitus, Type 1AnimalsGanglia, SpinalGene ExpressionMiceMice, Inbred C57BLMice, Inbred NODRNA, MessengerRNA, Messengerautoimmune diseases/disordersdorsal root ganglionneural regulationneurodegenerationNOD mouse/miceparasympathetic functiontype 1 diabetes

Identifiers

PMID37334284
PMCPMC10272810
OpenAlexW4379232995

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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.