Project description:Circular RNA microarray was performed to profile the circular RNA transcriptome of mouse MOVAS cells with or without benzo[a]pyrene (BaP) treatment. MOVAS cells were exposed to 10 μM BaP for 72 hours, and untreated MOVAS cells were used as control, with three biological replicates for each group (6 samples in total). Total RNA extracted from all samples was digested with RNase R to eliminate linear RNAs and enrich circular RNAs, followed by amplification and Cy3 fluorescent labeling using Arraystar Super RNA Labeling Kit. Labeled cRNAs were hybridized onto Arraystar Mouse circRNA Array V2 microarrays. Slides were scanned with Agilent Scanner G2505C, and raw intensity data were extracted via Agilent Feature Extraction software v11.0.1.1. Quantile normalization was conducted using the limma package in R. This submission contains raw and normalized microarray expression data only. The data provides a complete circRNA expression baseline for subsequent exploration of molecular mechanisms underlying BaP-induced vascular cell injury.

2026-07-05 | GSE337058 | GEO

Elucidating the Effects of the Environmental Pollutant Benzo[a]pyrene [BaP] on Cardiac Arrhythmogenicity

Project description:Benzo[a]pyrene (BaP) is a product of combustion and is an abundant constituent of wildfire derived smoke and particulate matter 2.5 (PM2.5). Although arrythmias are associated with wildfire, the mechanism remains unclear. We hypothesized that BaP might predispose individuals to arrhythmias and possibly sudden cardiac death. Human induced pluripotent stem cell-derived cardiomyocytes (iPSC-CMs) from healthy donors (n=3) were used to investigate the cardiovascular toxicity of BaP. Across a broad concentration range, BaP did not affect iPSC-CM viability, and a 4-day exposure of BaP at 50 M did not affect contractility. After exposure to BaP at 50 M for 5 days, iPSC-CMs were subjected to bulk RNA sequencing, and analysis revealed markers of inflammation were upregulated, and ion channel expression was modulated. Because inflammation is associated with reactive oxygen species (ROS) production, iPSC-CMs exposed to BaP had a concentration-dependent increase in ROS production. Mitotracker fluorescent imaging revealed decreased mitochondrial membrane potentials after iPSC-CMs treatment with 50 μM BaP. Seahorse assays revealed that BaP exposure decreased oxygen consumption rate, basal respiration, and maximal respiration in a dose-dependent manner. Using multiple electrode array (MEA) assays, iPSC-CMs exposed to 50 M BaP for 3 days, had prolonged field potential duration (FPD) and increased beat period (BP). However, co-treatment with N-acetyl cysteine (NAC), a nucleophile that scavenges ROS and preserves glutathione, attenuated the effect of BaP on FPD and BP (p<0.001). In summary, BaP exposure upregulated inflammatory cytokines and increased ROS production by impairing mitochondrial function. BaP had proarrhythmic effects of increased BP and FPD and was abrogated by NAC. Thus, BaP inhalation from wildfire smoke may predispose individuals to QT prolongation, arrhythmia, and sudden cardiac death.

2024-08-25 | GSE244567 | GEO

Predicting the in vivo developmental toxicity of benzo[a]pyrene (BaP) in rats by an in vitro-in silico approach.

Project description: Not available

| S-EPMC8448719 | biostudies-literature