Abstract
Bisphenol A (BPA) is a widely utilized endocrine disruptor capable of mimicking endogenous hormones, employed in the manufacture of numerous consumer products, thereby interfering with physiological cellular functions. Recent research has shown that BPA alters epigenetic cellular mechanisms in mammals and may be correlated to enhanced cellular senescence. Here, the effects of BPA at 10 ng/mL and 1 µg/mL, concentrations found in human samples, were analyzed on HT29 human colon adenocarcinona cell line and Human Umbilical Vein Endothelial Cells (HUVEC). Quantitative Real-Time Polymerase Chain Reaction (qRT-PCR) transcriptional analysis of the Long Interspersed Element-1 (LINE-1) retroelement showed that BPA induces global transcription deregulation in both cell lines, although with more pronounced effects in HUVEC cells. Whereas there was an increase in global transcription in HT29 exclusively after 24 h of exposure, this chemical had prolonged effects on HUVEC. Immunoblotting revealed that this was not accompanied by alterations in the overall content of H3K9me2 and H3K4me3 epigenetic marks. Importantly, cell viability assays and transcriptional analysis indicated that prolonged BPA exposure affects aging processes in senescent HUVEC. To our knowledge this is the first report that BPA interferes with senescence in primary vascular endothelial cells, therefore, suggesting its association to the etiology of age-related human pathologies, such as atherosclerosis.
Highlights
Bisphenol A (BPA) is an industrial chemical, employed in the manufacture of many consumer products such as polycarbonate plastics and epoxy resins
To access BPA effects on HT29 and Human Umbilical Vein Endothelial Cells (HUVEC) cells global transcription, we evaluated the expression of two distinct regions of Long Interspersed Element-1 (LINE-1) [24]
Considering that the main route of BPA exposure in humans occurs via ingestion followed by entrance into blood circulation, HT29 cell line and HUVEC were utilized as representatives of digestive tract and vascular tissues, respectively
Summary
Bisphenol A (BPA) is an industrial chemical, employed in the manufacture of many consumer products such as polycarbonate plastics and epoxy resins. Several studies show that BPA at very low concentrations alters proliferation kinetics and expression of cell cycle related genes, (e.g., [7,8]). BPA exposure can affect DNA methylation and gene expression [9]. Altered transcription patterns associated with modifications in DNA methylation have been reported for several genes in human cells exposed to BPA [12]. One report revealed that increased expression of the histone methyltransferase enhancer of Zeste Homolog 2 (EZH2) is induced by BPA with consequent increase in the overall level of histone H3 trimethylation at lysine 27 (H3K27me3), both in human breast cancer cells and in mouse mammary glands [13]. BPA effects on cellular viability and expression of senescence associated genes were analyzed on aging HUVEC cells
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