Evidence map›Paper›PMID 37446147›Full record

ArticleInternational journal of molecular sciences2023

A Novel Ex Vivo Model to Study Therapeutic Treatments for Myelin Repair following Ischemic Damage.

Luisa Werner, Michael Gliem, Nicole Rychlik, Goran Pavic, Laura Reiche, Frank Kirchhoff, Markley Silva Oliveira Junior, Joel Gruchot, Sven G Meuth, Patrick Küry and 1 more

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2023. 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
0.4field-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

3 citing papers in PubMed, 3 citations in OpenAlex.

  1. Article
  2. Article
  3. 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

11 authors at 2 institutions in 1 country.

Luisa WernerDepartment of Neurology, Medical Faculty, Heinrich Heine University, 40225 Düsseldorf, Germany.
Michael GliemDepartment of Neurology, Medical Faculty, Heinrich Heine University, 40225 Düsseldorf, Germany.
Nicole RychlikDepartment of Neurology, Medical Faculty, Heinrich Heine University, 40225 Düsseldorf, Germany.
Goran PavicDepartment of Neurology, Medical Faculty, Heinrich Heine University, 40225 Düsseldorf, Germany.ORCID 0000-0002-8104-1108
Laura ReicheDepartment of Neurology, Medical Faculty, Heinrich Heine University, 40225 Düsseldorf, Germany.ORCID 0000-0002-2358-9925
Frank KirchhoffMolecular Physiology, Center for Integrative Physiology and Molecular Medicine, University of Saarland, 66424 Homburg, Germany.ORCID 0000-0002-2324-2761
Markley Silva Oliveira JuniorDepartment of Neurology, Medical Faculty, Heinrich Heine University, 40225 Düsseldorf, Germany.ORCID 0000-0002-0631-4065
Joel GruchotDepartment of Neurology, Medical Faculty, Heinrich Heine University, 40225 Düsseldorf, Germany.ORCID 0000-0003-4894-4679
Sven G MeuthDepartment of Neurology, Medical Faculty, Heinrich Heine University, 40225 Düsseldorf, Germany.
Patrick KüryDepartment of Neurology, Medical Faculty, Heinrich Heine University, 40225 Düsseldorf, Germany.ORCID 0000-0002-2654-1126
Peter GöttleDepartment of Neurology, Medical Faculty, Heinrich Heine University, 40225 Düsseldorf, Germany.ORCID 0000-0001-6830-0956
Heinrich Heine University Düsseldorf · DESaarland University · DE

Funding

Christiane and Claudia Hempel Foundation for clinical stem cell research n.a.James and Elisabeth Cloppenburg, Peek and Cloppenburg Düsseldorf Stiftung n.a.
6 · The paper itself

Abstract

Stroke is a major reason for persistent disability due to insufficient treatment strategies beyond reperfusion, leading to oligodendrocyte death and axon demyelination, persistent inflammation and astrogliosis in peri-infarct areas. After injury, oligodendroglial precursor cells (OPCs) have been shown to compensate for myelin loss and prevent axonal loss through the replacement of lost oligodendrocytes, an inefficient process leaving axons chronically demyelinated. Phenotypic screening approaches in demyelinating paradigms revealed substances that promote myelin repair. We established an ex vivo adult organotypic coronal slice culture (OCSC) system to study repair after stroke in a resource-efficient way. Post-photothrombotic OCSCs can be manipulated for 8 d by exposure to pharmacologically active substances testing remyelination activity. OCSCs were isolated from a NG2-CreERT2-td-Tomato knock-in transgenic mouse line to analyze oligodendroglial fate/differentiation and kinetics. Parbendazole boosted differentiation of NG2

Indexed as

Demyelinating DiseasesStrokeAnimalsCell DifferentiationIschemiaMiceMice, TransgenicMyelin SheathOligodendrogliaischemic strokemyelin repairneuroregenerationoligodendrocyte

Identifiers

PMID37446147
PMCPMC10341986
OpenAlexW4382751813

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.