کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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5534332 | 1550840 | 2017 | 12 صفحه PDF | دانلود رایگان |
- Perinatal BPA exposure decreased β-Cas gene expression independently of PRL signaling.
- BPA altered the expression of HDAC1, HDAC3 and EZH2 in the lactating mammary gland.
- BPA induced acetylation and methylation of histones in the β-Cas gene.
- BPA induced changes in the DNA methylation status of the β-Cas gene.
With the aim to analyze whether bisphenol A (BPA) modifies β-Casein (β-Cas) synthesis and transcriptional regulation in perinatally exposed animals, here, pregnant F0 rats were orally exposed to 0, 0.6 or 52 μg BPA/kg/day from gestation day 9 until weaning. Then, F1 females were bred and mammary glands were obtained on lactation day 2. Perinatal BPA exposure decreased β-Cas expression without modifying the activation of prolactin receptor. It also decreased the expression of glucocorticoid receptor in BPA52-exposed dams and β1 and α6 integrins as well as dystroglycan in both BPA groups. In addition, BPA exposure altered the expression of histone-modifying enzymes and induced histone modifications and DNA methylation in the promoter, enhancer and exon VII of the β-Cas gene. An impaired crosstalk between the extracellular matrix and lactogenic hormone signaling pathways and epigenetic modifications of the β-Cas gene could be the molecular mechanisms by which BPA decreased β-Cas expression.
Journal: Molecular and Cellular Endocrinology - Volume 439, 5 January 2017, Pages 407-418