Evidence map›Paper›PMID 40134232›Full record

ArticleGlia2025

The Histone Methyltransferases EHMT1 and EHMT2 Repress the Expression of Genes Related to Excitability and Cell Death in Oligodendrocyte Progenitors.

Mathilde Pruvost, Hye-Jin Park, Chloé Habermacher, Meng Li, Maria Cecilia Angulo, Jia Liu, Patrizia Casaccia

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Glia, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. 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

7 authors.

Mathilde PruvostNeuroscience Initiative at the Advanced Science Research Center of the Graduate Center of the City University of New York, New York, New York, USA.ORCID 0000-0003-0844-7731
Hye-Jin ParkNeuroscience Initiative at the Advanced Science Research Center of the Graduate Center of the City University of New York, New York, New York, USA.
Chloé HabermacherUniversité Paris Cité, Institute of Psychiatry and Neuroscience of Paris (IPNP), INSERM U1266, Paris, France.
Meng LiNorris Medical Library, University of Southern California, Los Angeles, California, USA.
Maria Cecilia AnguloUniversité Paris Cité, Institute of Psychiatry and Neuroscience of Paris (IPNP), INSERM U1266, Paris, France.
Jia LiuNeuroscience Initiative at the Advanced Science Research Center of the Graduate Center of the City University of New York, New York, New York, USA.ORCID 0000-0001-6274-2710
Patrizia CasacciaNeuroscience Initiative at the Advanced Science Research Center of the Graduate Center of the City University of New York, New York, New York, USA.ORCID 0000-0002-4785-9264

Funding

Environmental Biosensors in the Oligodendrocyte LineageR35NS111604 · NINDS · ADVANCED SCIENCE RESEARCH CENTER · PI Patrizia Casaccia · 2019 to 2026
$9.1M
Agence Nationale de la Recherche ANR-21-CE37-0020-01Fondation de France R24040KKFondation pour l'Aide à la Recherche sur la Sclérose en PlaquesFondation pour la Recherche Médicale MND202310017891National Multiple Sclerosis Society FG-1907-34565NINDS NIH HHS R35 NS111604NINDS NIH HHS R35-NS111604
6 · The paper itself

Abstract

Oligodendrocyte progenitor cells (OPCs) represent a population of electrically active and dividing cells, which are capable of responding to neuronal activity by proliferating and differentiating. Here, we report that the repressive euchromatic H3K9me2 histone mark, deposited by the histone methyltransferases EHMT1 and EHMT2 enzymes, increases in proliferating OPCs in mice following optogenetic stimulation of neuronal activity. Using primary cultured OPCs with genetic deletion of Ehmt1 and Ehmt2, and pharmacological inhibition of EHMT enzymatic activity, we reveal the importance of these enzymes in repressing the expression of genes regulating cell death and electrical properties in proliferating OPCs. Consistent with these findings, we detect higher levels of cholinergic muscarinic receptors, fewer numbers of oligodendrocyte lineage cells, and lower levels of the myelin basic protein (MBP) in mice with lineage-specific ablation of Ehmt1 and Ehmt2. Together these data suggest that the repressive H3K9me2 histone mark, whose levels increase in proliferating OPCs after neuronal stimulation, is an important modulator of cell death and proteins regulating the electrical properties of OPCs.

Indexed as

Cell DeathHistocompatibility AntigensHistone-Lysine N-MethyltransferaseOligodendrocyte Precursor CellsOligodendrogliaAnimalsCell ProliferationCells, CulturedHistonesMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicG9a protein, mouseGLP protein, mouseHistocompatibility AntigensHistone-Lysine N-MethyltransferaseHistonesbrainchromatinepigeneticsG9aGlpneuronal stimulation

Identifiers

PMID40134232
PMCPMC12122236

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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.