Aerobic bacterial enrichment cultures that degraded BPA andits transformation products
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ABSTRACT:
PROVIDER: PRJNA1170533 | ENA |
REPOSITORIES: ENA
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Project description:Bisphenol A, an endocrine-disrupting compound, is used widely in the industrial production of plastic products. Despite increasing concerns about its harmful effects on human health, animals and the environment, the use of BPA has been banned only in infant products and its effects on cellular processes are not fully understood. To investigate the impact of BPA on eukaryotic cells, we analyzed proteome changes of wild-type and PDR5-deleted S. cerevisiae strains exposed to different doses of BPA using sample multiplexing-based quantitative mass spectrometry. We found that the ABC multidrug transporter Pdr5 plays an important role in protecting yeast cells from BPA toxicity, with its absence significantly sensitizes cells to BPA. BPA inhibited yeast growth in a dose-dependent manner, with a more pronounced effect in PDR5-deleted cells. Proteomic analysis revealed that BPA induces dose-dependent widespread changes in protein abundance, including the up-regulation of metabolic pathways such as arginine biosynthesis and the down-regulation of mitochondrial proteins. Additionally, we observed markers of cellular stress induced by BPA by identifying multiple stress-induced proteins up-regulated by this compound. As cellular processes affected by BPA have been shown to be evolutionary conserved, these insights can advance our understanding of BPA’s cellular impact and its broader effects on human health.
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Project description:Perinatal exposure to bisphenol A (BPA) has been shown to cause aberrant mammary gland morphogenesis and mammary neoplastic transformation. Yet, the underlying mechanism is poorly understood. We tested the hypothesis that mammary glands exposed to BPA during a susceptible window may lead to its susceptibility to tumorigenesis through a stem-cell mediated mechanism. We exposed 21-day-old Balb/c mice to BPA by gavage (25 µg/kg/day) during puberty for 3 weeks, and a subset of animals were further challenged with one oral dose (30 mg/kg) of 7,12-dimethylbenz[a]anthracene (DMBA) at 2 months of age. Primary mammary cells were isolated at 6 weeks, and 2 and 4 months of age for mammary stem cell (MaSC) quantification and function analysis. Pubertal exposure to the low-dose BPA increased lateral branches and hyperplasia in adult mammary glands and caused an acute increase of MaSC in 6-week-old glands and a delayed increase of luminal progenitors in 4-month-old adult gland. Most importantly, pubertal BPA exposure altered the function of MaSC from different age groups, causing pre-neoplastic lesions in their regenerated glands similar to those induced by DMBA exposure, which indicates that MaSCs are susceptible to BPA-induced transformation. Deep sequencing analysis on MaSC-enriched mammospheres identified a set of aberrantly expressed genes associated with pre-neoplastic lesions in human breast cancer patients. Thus, our study for the first time shows that pubertal BPA exposure altered MaSC gene expression and function such that they induced early neoplastic transformation.
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