Evidence map›Paper›PMID 27391474›Full record

ArticleJournal of neuroinflammation2016

Antibodies to the RNA-binding protein hnRNP A1 contribute to neurodegeneration in a model of central nervous system autoimmune inflammatory disease.

Joshua N Douglas, Lidia A Gardner, Hannah E Salapa, Stephen J Lalor, Sangmin Lee, Benjamin M Segal, Paul E Sawchenko, Michael C Levin

Open access · goldAbstract read
In one paragraph

Article in Journal of neuroinflammation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.5field-weighted citation impact, top 12% 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

16 citing papers in PubMed, 32 citations in OpenAlex.

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  11. Differential modulation of Ahr and Arid5a: A promising therapeutic strategy for autoimmune encephalomyelitis.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2020
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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 4 institutions in 1 country.

Joshua N DouglasDepartment of Neurology, University of Tennessee Health Science Center, 855 Monroe Avenue, Room 415, Memphis, TN, 38163, USA.
Lidia A GardnerResearch Service, VA Medical Center, Memphis, TN, USA.
Hannah E SalapaDepartment of Neurology, University of Tennessee Health Science Center, 855 Monroe Avenue, Room 415, Memphis, TN, 38163, USA.
Stephen J LalorDepartment of Neurology, University of Michigan Medical School, Ann Arbor, MI, USA.
Sangmin LeeResearch Service, VA Medical Center, Memphis, TN, USA.
Benjamin M SegalDepartment of Neurology, University of Michigan Medical School, Ann Arbor, MI, USA.
Paul E SawchenkoLaboratory of Neuronal Structure & Function, The Salk Institute, La Jolla, CA, USA.
Michael C LevinResearch Service, VA Medical Center, Memphis, TN, USA. mlevin@uthsc.edu.
University of Tennessee Health Science Center · USUniversity of Michigan–Ann Arbor · USMemphis VA Medical Center · USSalk Institute for Biological Studies · US

Funding

Molecular Mimicry in Immune Mediated Neurologic DiseaseI01BX001996 · VA · MEMPHIS VA MEDICAL CENTER · PI TSAO, JACK W · 2013 to 2020
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BLRD VA I01 BX001996
6 · The paper itself

Abstract

backgroundNeurodegeneration is believed to be the primary cause of permanent, long-term disability in patients with multiple sclerosis. The cause of neurodegeneration in multiple sclerosis appears to be multifactorial. One mechanism that has been implicated in the pathogenesis of neurodegeneration in multiple sclerosis is the targeting of neuronal and axonal antigens by autoantibodies. Multiple sclerosis patients develop antibodies to the RNA-binding protein, heterogeneous nuclear ribonucleoprotein A1 (hnRNP A1), which is enriched in neurons. We hypothesized that anti-hnRNP A1 antibodies would contribute to neurodegeneration in an animal model of multiple sclerosis.

methodsFollowing induction of experimental autoimmune encephalomyelitis (EAE) by direct immunization with myelin oligodendrocyte glycoprotein, mice were injected with anti-hnRNP A1 or control antibodies. Animals were examined clinically, and the central nervous system (CNS) tissues were tested for neurodegeneration with Fluoro-Jade C, a marker of degenerating neural elements.

resultsInjection of anti-hnRNP A1 antibodies in mice with EAE worsened clinical disease, altered the clinical disease phenotype, and caused neurodegeneration preferentially in the ventral spinocerebellar tract and deep white matter of the cerebellum in the CNS. Neurodegeneration in mice injected with hnRNP A1-M9 antibodies compared to control groups was consistent with "dying back" axonal degeneration.

conclusionsThese data suggest that antibodies to the RNA-binding protein hnRNP A1 contribute to neurodegeneration in immune-mediated disease of the CNS.

Indexed as

AnimalsAutoantibodiesEncephalomyelitis, Autoimmune, ExperimentalFemaleHeterogeneous Nuclear Ribonucleoprotein A1Heterogeneous-Nuclear Ribonucleoprotein Group A-BMiceMice, Inbred C57BLNeurodegenerative DiseasesAutoantibodiesHeterogeneous Nuclear Ribonucleoprotein A1Heterogeneous-Nuclear Ribonucleoprotein Group A-BHnrnpa1 protein, mouseExperimental autoimmune encephalomyelitishnRNP A1Multiple sclerosisNeurodegenerationRNA-binding protein

Identifiers

PMID27391474
PMCPMC4938923
OpenAlexW2471157725

What OpenQuestion holds

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LicenceCC BY
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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.