Dataset Information

Transcriptomic changes in human AC16 cardiomyocytes induced by electronic cigarette aerosol exposure

ABSTRACT: Electronic cigarette (e-cig) use has raised increasing concerns regarding its cardiovascular effects, yet the underlying molecular mechanisms in cardiomyocytes remain unclear. In this study, human AC16 cardiomyocytes were exposed to e-cigarette aerosol using an air–liquid interface system, and transcriptomic profiling was performed to identify differentially expressed miRNAs and mRNAs. The analysis revealed marked alterations in calcium signaling–related genes, most notably suppression of miR-6504-3p and upregulation of its target gene PLN, providing mechanistic insight into e-cig–induced cardiomyocyte injury.

ORGANISM(S): Homo sapiens

PROVIDER: GSE338719 | GEO | 2026/07/20

REPOSITORIES: GEO

ACCESS DATA

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Project description:Electronic cigarettes (E-cigs) represent a rapidly growing public health concern, particularly due to their widespread adoption among adolescents. Recent epidemiological and experimental evidence has linked E-cig use to accelerated atherosclerosis, though the underlying mechanisms remain incompletely understood. Here, we investigated how E-cig exposure promotes atherosclerotic lesion formation and vascular remodeling through phenotypic modulation of vascular smooth muscle cells (SMCs). We utilized SMC lineage-tracing mice crossed onto an ApoE-null hyperlipidemic background and exposed them to pod-based E-cigs (Juul) three times weekly over a 12-week period (n=16 per group), comparing results to control mice exposed to Ambient air. Single-cell RNA sequencing (scRNA-seq) and assay for transposase-accessible chromatin sequencing (scATAC-seq) were conducted on cells isolated from the aortic sinus, complemented by histological assessment of osteogenic markers. Our analyses revealed a significant shift in SMC phenotype toward a chondrogenic lineage (CMC) in e-cigarette-exposed mice, evidenced by markedly increased expression of chondrogenic markers Col2a1 and Tnfrsf11b. Correspondingly, histological evaluations demonstrated increased osteogenic activity in E-cig-exposed animals. Chromatin accessibility profiling further identified a unique cellular cluster enriched for glutamatergic signaling pathways, particularly showing enhanced accessibility at Grin2a, a gene encoding the NMDA receptor subunit GluN2A. Notably, GRIN2A expression was upregulated in HCASMCs upon e-cigarette exposure, and the observed E-cig-induced phenotypic modulation was found to be GRIN2A-dependent, suggesting a robust gene-environment interaction. Collectively, these findings elucidate critical mechanistic pathways through which e-cigarette exposure promotes atherosclerosis, underscoring GRIN2A as a potential therapeutic target to address cardiovascular risks associated with electronic nicotine delivery systems.

Dataset Information

Transcriptomic changes in human AC16 cardiomyocytes induced by electronic cigarette aerosol exposure

Dataset's files

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets