Evidence map›Paper›PMID 20720108›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2010

Mechanisms of regulation of oligodendrocyte development by p38 mitogen-activated protein kinase.

Li-Jin Chew, William Coley, Ying Cheng, Vittorio Gallo

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
3.7field-weighted citation impact, top 7% 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

57 citing papers in PubMed, 91 citations in OpenAlex.

  1. Review
  2. LY2940094, an NOPR antagonist, promotes oligodendrocyte generation and myelin recovery in an NOPR independent manner.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2024
    Article
  3. Regulators of Oligodendrocyte Differentiation.Cold Spring Harbor perspectives in biology · 2024
    Review
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  15. Murine Esophagus Expresses Glial-Derived Central Nervous System Antigens.International journal of molecular sciences · 2021
    Article
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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

4 authors at 1 institution in 1 country.

Li-Jin ChewCenter for Neuroscience Research, Children's Research Institute, Children's National Medical Center, Washington, DC 20010, USA. lchew@cnmcresearch.org
William Coley
Ying Cheng
Vittorio Gallo
Children's National · US

Funding

Characterization of Sox17 as a Regulator of Oligodendrocyte Cell DifferentiationR01NS056427 · NINDS · CHILDREN'S RESEARCH INSTITUTE · PI VITTORIO GALLO, VITTORIO GALLO VITTORIO GALLO · 2007 to 2011
$1.8M
NINDS NIH HHS R01 NS056427
6 · The paper itself

Abstract

Many extracellular and intrinsic factors regulate oligodendrocyte development, but their signaling pathways remain poorly understood. Although the p38 mitogen-activated protein kinase (MAPK)-dependent pathway is implicated in oligodendrocyte progenitor cell (OPC) lineage progression, its molecular targets involved in myelinogenesis are mostly unidentified. We have analyzed mechanisms by which p38MAPK regulates oligodendrocyte development and demonstrate that p38MAPK inhibition prevents OPC lineage progression and inhibits MBP (myelin basic protein) promoter activity and Sox10 function. In white-matter tissue, differential levels of MAPK phosphorylation are observed in oligodendrocyte lineage cells. Phosphorylated p38MAPK was found in CC1- and CNP-expressing differentiated oligodendrocytes of the adult brain and was temporally associated with a decline in the levels of phosphorylated extracellular signal-regulated kinase (ERK) in cells of this lineage. PDGF stimulates the phosphorylation of ERK, p38MAPK, and c-Jun N-terminal kinase (JNK), and p38MAPK inhibition was associated with increased ERK, JNK, and c-Jun phosphorylation. In the presence of PDGF, simultaneous inhibition of p38MAPK and either MAPK kinase (MEK) or JNK significantly alleviates the repression of myelin gene expression and lineage progression induced by p38MAPK inhibition alone. Dominant-negative c-Jun reverses the inhibition of myelin promoter activity by active MEK1 or dominant-negative p38MAPKalpha mutants, and phosphorylated c-Jun was detected at the MBP promoter after p38MAPK inhibition, indicating c-Jun as a negative mediator of p38MAPK action. Our findings indicate that p38MAPK activity in the brain supports myelin gene expression through distinct mechanisms via positive and negative regulatory targets. We show that oligodendrocyte differentiation involves p38-mediated Sox10 regulation and cross talk with parallel ERK and JNK pathways to repress c-Jun activity.

Indexed as

MAP Kinase Signaling SystemAnimalsBrainCell LineageCell ProliferationCell SurvivalDNAMiceMitogen-Activated Protein Kinase KinasesMyelin Basic ProteinNerve Fibers, MyelinatedNerve Tissue ProteinsOligodendrogliap38 Mitogen-Activated Protein KinasesPhosphoric Monoester HydrolasesPhosphorylationDNAMbp protein, mouseMitogen-Activated Protein Kinase KinasesMyelin Basic ProteinNerve Tissue Proteinsp38 Mitogen-Activated Protein KinasesPhosphoric Monoester HydrolasesSox10 protein, mouseSOXE Transcription FactorsTranscription Factors

Identifiers

PMID20720108
PMCPMC3327889
OpenAlexW1978855174

What OpenQuestion holds

Textmetadata
LicenceTDM
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.