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

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

PROVIDER: PRJNA1023581 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26272517_1.fastq.gz	Fastqsanger.gz
	SRR26272517_2.fastq.gz	Fastqsanger.gz
	SRR26272518_1.fastq.gz	Fastqsanger.gz
	SRR26272518_2.fastq.gz	Fastqsanger.gz
	SRR26272519_1.fastq.gz	Fastqsanger.gz

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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

MicroRNA expression profiling in adult mouse liver following benzo(a)pyrene (BaP) treatment [Agilent miRNA array]

Project description:Lack of change in microRNA expression in adult mouse liver following treatment with benzo(a)pyrene (BaP), as detected using Agilent miRNA arrays. We have investigated the effect of exposure to 150 mg/kg benzo(a)pyrene (BaP) for 3 days on mRNA and miRNA expression levels in adult mouse liver. We used Agilent miRNA array platforms to assess effects of BaP exposure on miRNA expression levels. Our results indicate a distinct lack of effect of BaP of miRNA expression, despite widespread changes in mRNA levels. Keywords: Toxicology, miRNA

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MicroRNA expression profiling in adult mouse liver following benzo(a)pyrene (BaP) treatment [Exiqon miRNA array]

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Toxicogenomics and phenotypic characterization of adult male zebrafish liver treated with benzo-[A]-pyrene (BAP)

Project description:We performed microarray-based expression profiling on liver of male zebrafish exposed to 5, 50, and 500 µg/L of benzo-[A]-pyrene (BAP) for 24 and 96 hours, to identify global transcriptional programs and biological pathways involved in BAP-induced adaptive responses under in vivo environment.

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Toxicogenomics and phenotypic characterization of adult male zebrafish liver treated with benzo-[A]-pyrene (BAP)

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Project description:Benzo(a)pyrene (Bap), a key component of cigarette smoke (CS), is a pollutant and widely present in our daily life. The roles of Bap on viral replication have been amply discussed and controversial. In our present study, we investigated the effect and mechanism of Bap on the replication of vesicular stomatitis virus (VSV) and respiratory syncytial virus (RSV) in vitro. HeLa cells were pre-exposed to Bap at 10 μM for 48 h and then infected with VSV (MOI=1) for 24 h. RNA sequencing analysis was conducted to identify Bap-dysregulated genes and qPCR analysis was used to identify the result. Chronic exposed to Bap significantly inhibited the replication of VSV and RSV in vitro and in vivo.

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MicroRNA expression profiling in adult mouse liver following benzo(a)pyrene (BaP) treatment [Exiqon miRNA array]

Project description:Lack of change in microRNA expression in adult mouse liver following treatment with benzo(a)pyrene (BaP), as detected using Exiqon miRNA arrays. Adult male mice were exposed to 150 mg/kg benzo(a)pyrene (BaP) or solvent for 3 days and sampled 4 hours after the last dose. MicroRNA expression levels in adult mouse liver were measured using Exiqon miRNA arrays. Our results indicate a distinct lack of effect of BaP of miRNA expression, despite widespread changes in mRNA levels (measured using Agilent arrays). Lack of miRNA changes was confirmed with Agilent miRNA arrays. Keywords: Toxicology, miRNA Adult male B6C3F1 mice were exposed to a daily dose of corn oil (vehicle control group) or 150 mg/kg BaP (treatment group) for 3 d (n=6 per group). Mice were sacrificed at 4 h or 24 h following the last dose and liver lobes were extracted and flash frozen. Exiqon miRNA arrays were used to examine changes in miRNA transcript levels in random liver lobe sections.

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mRNA expression profiling in adult mouse liver following benzo(a)pyrene (BaP) treatment [Agilent gene expression array]

Project description:Adult male mice were exposed to 150 mg/kg benzo(a)pyrene (BaP) or solvent for 3 days and sampled 4 or 24 hours after the last dose. mRNA expression levels in adult mouse liver were measured using Agilent arrays. We found widespread changes in mRNA in pathways consistent with known response (xenobiotic metabolism, glutathione). We also found that BaP caused changes in the circadian rhythm pathway. We measured miRNA changes in the same samples and found no evidence for any change in transcription of miRNA as a result of the exposure. Keywords: Toxicology, time course

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Microarray data of benzo[a]pyrene-treated WHCO1 vs EPC-2 cells

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HepG2 cells exposed to Benzo[a]pyrene for 6,12,18,24,36 and 48h.

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