Comp Biochem Physiol C Toxicol Pharmacol. 2026 Apr 2:110534. doi: 10.1016/j.cbpc.2026.110534. Online ahead of print.
ABSTRACT
Sodium p-perfluorous nonenoxybenzenesulfonate (OBS), an emerging alternative to perfluorooctane sulfonate (PFOS), has raised public health concerns due to its potential cardiovascular toxicity, but the underlying epigenetic mechanisms remain poorly characterized. This study aimed to elucidate the miRNA-mRNA regulatory networks involved in OBS-induced endothelial dysfunction in human umbilical vein endothelial cells (HUVECs). Integrated transcriptomic and miRNA-sequencing analysis identified 685 differentially expressed genes (DEGs) and 74 differentially expressed miRNAs (DEMs) in HUVECs exposed to OBS exposure (20 μmol/L, 48 h). miRNA target genes were predicted by intersecting three databases (TargetScan, miRanda, and ENCORI) and then overlapped with the DEGs. Integrated analysis identified 25 key target genes, including 9 cardiovascular disease-associated genes that formed 8 miRNA-mRNA pairs exhibiting a negatively regulatory relationship. Functionally, OBS exposure significantly impaired endothelial cell migration, enhanced adhesion to the extracellular matrix, and triggered intracellular reactive oxygen species (ROS) accumulation. These phenotypic changes strongly correlated with perturbations in the identified miRNA-mRNA networks. Furthermore, disease enrichment analysis based on the DisGeNET database suggested potential links between the OBS-perturbed molecular networks and cardiovascular pathologies, such as cardiomyopathy and coronary artery disease. These findings provide the first epigenetic evidence that OBS exposure induces endothelial dysfunction via miRNA-mRNA regulatory networks, thereby implicating it as a potential cardiovascular hazard.
PMID:41935675 | DOI:10.1016/j.cbpc.2026.110534