Evidence map›Paper›PMID 33569054›Full record

ArticleFrontiers in immunology2020

RGC-32 Regulates Generation of Reactive Astrocytes in Experimental Autoimmune Encephalomyelitis.

Alexandru Tatomir, Austin Beltrand, Vinh Nguyen, Dallas Boodhoo, Armugam Mekala, Cornelia Cudrici, Tudor C Badea, Dafin F Muresanu, Violeta Rus, Horea Rus

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Frontiers in immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.5field-weighted citation impact, top 39% 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

4 citing papers in PubMed, 5 citations in OpenAlex.

  1. AFrontiers in immunology · 2023
    Article
  2. Review
  3. Review
  4. 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

10 authors at 5 institutions in 2 countries.

Alexandru TatomirDepartment of Neurology, University of Maryland, School of Medicine, Baltimore, MD, United States.
Austin BeltrandDepartment of Neurology, University of Maryland, School of Medicine, Baltimore, MD, United States.
Vinh NguyenDepartment of Medicine, Division of Rheumatology and Clinical Immunology, University of Maryland, School of Medicine, Baltimore, MD, United States.
Dallas BoodhooDepartment of Neurology, University of Maryland, School of Medicine, Baltimore, MD, United States.
Armugam MekalaDepartment of Neurology, University of Maryland, School of Medicine, Baltimore, MD, United States.
Cornelia CudriciTranslational Vascular Medicine Branch, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, MD, United States.
Tudor C BadeaRetinal Circuit Development and Genetics Unit, Neurobiology Neurodegeneration & Repair Laboratory (N-NRL), National Eye Institute, Bethesda, MD, United States.
Dafin F MuresanuDepartment of Neurosciences, "Iuliu Hatieganu" University of Medicine and Pharmacy, Cluj-Napoca, Romania.
Violeta RusDepartment of Medicine, Division of Rheumatology and Clinical Immunology, University of Maryland, School of Medicine, Baltimore, MD, United States.
Horea RusDepartment of Neurology, University of Maryland, School of Medicine, Baltimore, MD, United States.
University of Maryland, Baltimore · USIuliu Hațieganu University of Medicine and Pharmacy · RONational Eye Institute · USNational Institutes of Health · USVA Maryland Health Care System · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Astrocytes are increasingly recognized as critical contributors to multiple sclerosis pathogenesis. We have previously shown that lack of Response Gene to Complement 32 (RGC-32) alters astrocyte morphology in the spinal cord at the peak of experimental autoimmune encephalomyelitis (EAE), suggesting a role for RGC-32 in astrocyte differentiation. In this study, we analyzed the expression and distribution of astrocytes and astrocyte progenitors by immunohistochemistry in spinal cords of wild-type (WT) and RGC-32-knockout (KO) mice with EAE and of normal adult mice. Our analysis showed that during acute EAE, WT astrocytes had a reactive morphology and increased GFAP expression, whereas RGC-32 KO astrocytes had a morphology similar to that of radial glia and an increased expression of progenitor markers such as vimentin and fatty acid binding protein 7 (FABP7). In control mice, GFAP expression and astrocyte density were also significantly higher in the WT group, whereas the number of vimentin and FABP7-positive radial glia was significantly higher in the RGC-32 KO group.

Indexed as

Cell ProliferationAnimalsAstrocytesCell DifferentiationCell MovementCells, CulturedEncephalomyelitis, Autoimmune, ExperimentalFatty Acid-Binding Protein 7FemaleGlial Fibrillary Acidic ProteinMiceMice, Inbred C57BLMice, KnockoutNuclear ProteinsPhenotypeRatsFabp7 protein, mouseFatty Acid-Binding Protein 7Glial Fibrillary Acidic Proteinglial fibrillary astrocytic protein, mouseNuclear ProteinsRgc-32 protein, mouseVimentinVim protein, mouseastrocyteexperimental autoimmune encephalomyelitisFABP7GFAPradial gliaResponse Gene to Complement-32vimentin

Identifiers

PMID33569054
PMCPMC7868332
OpenAlexW3123740447

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.