Evidence map›Paper›PMID 31906095›Full record

ArticleCells2019

Csf1 Deficiency Dysregulates Glial Responses to Demyelination and Disturbs CNS White Matter Remyelination.

Bartosz Wylot, Jakub Mieczkowski, Sylwia Niedziolka, Bozena Kaminska, Malgorzata Zawadzka

Open access · goldAbstract read
In one paragraph

Article in Cells, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

18 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
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  6. CD11cCell death & disease · 2023
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  9. Review
  10. Article
  11. Review
  12. Microglial vesicles improve post-stroke recovery by preventing immune cell senescence and favoring oligodendrogenesis.Molecular therapy : the journal of the American Society of Gene Therapy · 2021
    Article
  13. Review
  14. Is Pre-Symptomatic Immunosuppression Protective in CSF1R-Related Leukoencephalopathy?Movement disorders : official journal of the Movement Disorder Society · 2021
    Article
  15. Article
  16. Article
  17. Review
  18. 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

5 authors at 1 institution in 1 country.

Bartosz WylotNencki Institute of Experimental Biology, 02-093, Warsaw, Poland.
Jakub MieczkowskiNencki Institute of Experimental Biology, 02-093, Warsaw, Poland.
Sylwia NiedziolkaNencki Institute of Experimental Biology, 02-093, Warsaw, Poland.
Bozena KaminskaNencki Institute of Experimental Biology, 02-093, Warsaw, Poland.
Malgorzata ZawadzkaNencki Institute of Experimental Biology, 02-093, Warsaw, Poland.
Instytut Biologii Doświadczalnej im. Marcelego Nenckiego · PL

Funding

2011/03/B/NZ4/02988 2011/03/B/NZ4/02988
6 · The paper itself

Abstract

Remyelination, a highly efficient central nervous system (CNS) regenerative process, is performed by oligodendrocyte progenitor cells (OPCs), which are recruited to the demyelination sites and differentiate into mature oligodendrocytes to form a new myelin sheath. Microglia, the specialized CNS-resident phagocytes, were shown to support remyelination through secretion of factors stimulating OPC recruitment and differentiation, and their pharmacological depletion impaired remyelination. Macrophage colony-stimulating factor (Csf1) has been implicated in the control of recruitment and polarization of microglia/macrophages in injury-induced CNS inflammation. However, it remains unclear how Csf1 regulates a glial inflammatory response to demyelination as well as axonal survival and new myelin formation. Here, we have investigated the effects of the inherent Csf1 deficiency in a murine model of remyelination. We showed that remyelination was severely impaired in Csf1-/- mutant mice despite the fact that reduction in monocyte/microglia accumulation affects neither the number of OPCs recruited to the demyelinating lesion nor their differentiation. We identified a specific inflammatory gene expression signature and found aberrant astrocyte activation in Csf1-/- mice. We conclude that Csf1-dependent microglia activity is essential for supporting the equilibrium between microglia and astrocyte pro-inflammatory vs. regenerative activation, demyelinated axons integration and, ultimately, reconstruction of damaged white matter.

Indexed as

AnimalsAstrocytesBiomarkersCell DifferentiationCell MovementDemyelinating DiseasesDisease Models, AnimalFluorescent Antibody TechniqueGene Expression ProfilingImmunophenotypingMacrophage Colony-Stimulating FactorMiceMice, TransgenicMicrogliaNeurogliaRemyelinationBiomarkersCSF1 protein, mouseMacrophage Colony-Stimulating FactorCsf1microgliaosteopetrotic miceremyelination

Identifiers

PMID31906095
PMCPMC7017166
OpenAlexW2998493548

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.