Evidence map›Paper›PMID 34920725›Full record

ArticleJournal of neuroinflammation2021

LPA

Fabian Szepanowski, Maximilian Winkelhausen, Rebecca D Steubing, Anne K Mausberg, Christoph Kleinschnitz, Mark Stettner

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 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.9field-weighted citation impact, top 22% 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

9 citing papers in PubMed, 12 citations in OpenAlex.

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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

6 authors at 1 institution in 1 country.

Fabian SzepanowskiDepartment of Neurology and Center for Translational Neuro- and Behavioral Sciences (C-TNBS), University Medicine Essen, University Duisburg-Essen, Hufelandstr. 55, 45147, Essen, Germany. fabian.szepanowski@uk-essen.de.
Maximilian WinkelhausenDepartment of Neurology and Center for Translational Neuro- and Behavioral Sciences (C-TNBS), University Medicine Essen, University Duisburg-Essen, Hufelandstr. 55, 45147, Essen, Germany.
Rebecca D SteubingDepartment of Neurology and Center for Translational Neuro- and Behavioral Sciences (C-TNBS), University Medicine Essen, University Duisburg-Essen, Hufelandstr. 55, 45147, Essen, Germany.
Anne K MausbergDepartment of Neurology and Center for Translational Neuro- and Behavioral Sciences (C-TNBS), University Medicine Essen, University Duisburg-Essen, Hufelandstr. 55, 45147, Essen, Germany.
Christoph KleinschnitzDepartment of Neurology and Center for Translational Neuro- and Behavioral Sciences (C-TNBS), University Medicine Essen, University Duisburg-Essen, Hufelandstr. 55, 45147, Essen, Germany.
Mark StettnerDepartment of Neurology and Center for Translational Neuro- and Behavioral Sciences (C-TNBS), University Medicine Essen, University Duisburg-Essen, Hufelandstr. 55, 45147, Essen, Germany.
University of Duisburg-Essen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLysophosphatidic acid (LPA) is a pleiotropic lipid messenger that addresses at least six specific G-protein coupled receptors. Accumulating evidence indicates a significant involvement of LPA in immune cell regulation as well as Schwann cell physiology, with potential relevance for the pathophysiology of peripheral neuroinflammation. However, the role of LPA signaling in inflammatory neuropathies has remained completely undefined. Given the broad expression of LPA receptors on both Schwann cells and cells of the innate and adaptive immune system, we hypothesized that inhibition of LPA signaling may ameliorate the course of disease in experimental autoimmune neuritis (EAN).

methodsWe induced active EAN by inoculation of myelin protein 2 peptide (P2

resultsLewis rats treated with AM095 displayed a significant improvement in clinical scores, most notably during the remission phase. Cellular infiltration of sciatic nerve was only discretely affected by AM095. Hemogram profiles indicated no impact on circulating leukocytes. However, sciatic nerve immunohistochemistry revealed a reduction in the number of Schwann cells expressing the dedifferentiation marker Sox2 paralleled by a corresponding increase in differentiating Sox10-positive Schwann cells. In line with this, morphometric analysis of sciatic nerve semi-thin sections identified a significant increase in large-caliber myelinated axons at 28 dpi. Myelin thickness was unaffected by AM095.

conclusionThus, LPA

Indexed as

AnimalsBiphenyl CompoundsCell DedifferentiationFemaleIsoxazolesNeuritis, Autoimmune, ExperimentalRatsRats, Inbred LewReceptors, Lysophosphatidic AcidSchwann CellsSignal TransductionAMO95Biphenyl CompoundsIsoxazolesReceptors, Lysophosphatidic AcidDemyelinationDifferentiationExperimental autoimmune neuritis (EAN)Guillain–Barré-syndromeInflammatory neuropathyLysophosphatidic acid (LPA)RemyelinationSchwann cellSox10Sox2

Identifiers

PMID34920725
PMCPMC8680309
OpenAlexW4200567520

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.