ArticleCommunications biology2025
Single-cell profiling of H3K4me1-H3K27me3 revealed bivalent regulation of abnormal neuronal development caused by prenatal e-cigarette vaporing.
Article in Communications biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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.
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Who cites it
1 citing paper in PubMed.
- E-cigarette aerosol-induced neurotoxicity during early brain development: mechanisms and outcomes.Pediatric research · 2026Review
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4 authors.
Funding
Abstract
Histone H3K4me1 and H3K27me3 modifications play a crucial role in regulating neuronal development by maintaining the balance between active and inactive genes during neurogenesis. Prenatal exposure to electronic-cigarette (e-cig) aerosol has been shown to alter neuronal differentiation in a neuron type-specific manner. However, it remains unclear whether e-cig aerosol exposure affects gene expression by altering H3K4me1 and H3K27me3 modifications. Using single-nucleus joint profiling of H3K4me1-H3K27me3 and transcriptome of neonatal rat prefrontal cortex, we demonstrate that e-cig aerosol exposure alters the H3K4me1-H3K27me3 methylation patterns in the promoters, i.e., the bivalency, of many cell type-specific genes, impacting gene expression levels, neuronal differentiation and functions. Additionally, the prenatal e-cig aerosol exposure impacts the expression of genes related to circadian entrainment, calcium signaling, protein kinase signaling transduction, and synaptic transmission. These results suggest that nicotine addiction may be epigenetically imprinted at a very early stage of brain development.
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