Koneva L A, Vyas A K, McEachin R C, Puttabyatappa M, Wang H-S, Sartor M A, Padmanabhan V
Departments of Computational Medicine and Bioinformatics, University of Michigan, Ann Arbor, Michigan.
Department of Pediatrics, Texas Tech Health Sciences Permian Basin, Odessa, Texas.
Environ Mol Mutagen. 2017 Jan;58(1):4-18. doi: 10.1002/em.22071. Epub 2017 Jan 12.
Epidemiologic studies and studies in rodents point to potential risks from developmental exposure to BPA on cardiometabolic diseases. Furthermore, it is becoming increasingly evident that the manifestation and severity of adverse outcomes is the result of interaction between developmental insults and the prevailing environment. Consistent with this premise, recent studies in sheep found prenatal BPA treatment prevented the adverse effects of postnatal obesity in inducing hypertension. The gene networks underlying these complex interactions are not known. mRNA-seq of myocardium was performed on four groups of four female sheep to assess the effects of prenatal BPA exposure, postnatal overfeeding and their interaction on gene transcription, pathway perturbations and functional effects. The effects of prenatal exposure to BPA, postnatal overfeeding, and prenatal BPA with postnatal overfeeding all resulted in transcriptional changes (85-141 significant differentially expressed genes). Although the effects of prenatal BPA and postnatal overfeeding did not involve dysregulation of many of the same genes, they affected a remarkably similar set of biological pathways. Furthermore, an additive or synergistic effect was not found in the combined treatment group, but rather prenatal BPA treatment led to a partial reversal of the effects of overfeeding alone. Many genes previously known to be affected by BPA and involved in obesity, hypertension, or heart disease were altered following these treatments, and AP-1, EGR1, and EGFR were key hubs affected by BPA and/or overfeeding. Environ. Mol. Mutagen. 58:4-18, 2017. © 2016 Wiley Periodicals, Inc.
流行病学研究以及对啮齿动物的研究表明,发育过程中接触双酚A(BPA)可能会引发心脏代谢疾病。此外,越来越明显的是,不良后果的表现和严重程度是发育损伤与当前环境相互作用的结果。基于这一前提,最近对绵羊的研究发现,产前BPA处理可预防产后肥胖诱发高血压的不良影响。这些复杂相互作用背后的基因网络尚不清楚。对四组四只雌性绵羊的心肌进行mRNA测序,以评估产前BPA暴露、产后过度喂养及其相互作用对基因转录、通路扰动和功能效应的影响。产前暴露于BPA、产后过度喂养以及产前BPA与产后过度喂养的联合作用均导致转录变化(85 - 141个显著差异表达基因)。虽然产前BPA和产后过度喂养的影响并不涉及许多相同基因的失调,但它们影响的生物通路却非常相似。此外,联合治疗组未发现相加或协同效应,相反,产前BPA处理导致单独过度喂养效应的部分逆转。许多先前已知受BPA影响且与肥胖、高血压或心脏病有关的基因在这些处理后发生了改变,AP - 1、EGR1和EGFR是受BPA和/或过度喂养影响的关键枢纽。《环境与分子突变》58:第4 - 18页,2017年。© 2016威利期刊公司