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000132912 1001_ $$aJunge, Kristin M$$b0
000132912 245__ $$aMEST mediates the impact of prenatal bisphenol A exposure on long-term body weight development.
000132912 260__ $$a[S.l.]$$bBioMed Central$$c2018
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000132912 520__ $$aExposure to endocrine-disrupting chemicals can alter normal physiology and increase susceptibility to non-communicable diseases like obesity. Especially the prenatal and early postnatal period is highly vulnerable to adverse effects by environmental exposure, promoting developmental reprogramming by epigenetic alterations. To obtain a deeper insight into the role of prenatal bisphenol A (BPA) exposure in children's overweight development, we combine epidemiological data with experimental models and BPA-dependent DNA methylation changes.BPA concentrations were measured in maternal urine samples of the LINA mother-child-study obtained during pregnancy (n = 552), and BPA-associated changes in cord blood DNA methylation were analyzed by Illumina Infinium HumanMethylation450 BeadChip arrays (n = 472). Methylation changes were verified by targeted MassARRAY analyses, assessed for their functional translation by qPCR and correlated with children's body mass index (BMI) z scores at the age of 1 and 6 years. Further, female BALB/c mice were exposed to BPA from 1 week before mating until delivery, and weight development of their pups was monitored (n ≥ 8/group). Additionally, human adipose-derived mesenchymal stem cells were treated with BPA during the adipocyte differentiation period and assessed for exposure-related epigenetic, transcriptional and morphological changes (n = 4).In prenatally BPA-exposed children two CpG sites with deviating cord blood DNA-methylation profiles were identified, among them a hypo-methylated CpG in the promoter of the obesity-associated mesoderm-specific transcript (MEST). A mediator analysis suggested that prenatal BPA exposure was connected to cord blood MEST promoter methylation and MEST expression as well as BMI z scores in early infancy. This effect could be confirmed in mice in which prenatal BPA exposure altered Mest promoter methylation and transcription with a concomitant increase in the body weight of the juvenile offspring. An experimental model of in vitro differentiated human mesenchymal stem cells also revealed an epigenetically induced MEST expression and enhanced adipogenesis following BPA exposure.Our study provides evidence that MEST mediates the impact of prenatal BPA exposure on long-term body weight development in offspring by triggering adipocyte differentiation.
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000132912 7001_ $$aLeppert, Beate$$b1
000132912 7001_ $$aJahreis, Susanne$$b2
000132912 7001_ $$aWissenbach, Dirk K$$b3
000132912 7001_ $$aFeltens, Ralph$$b4
000132912 7001_ $$0P:(DE-He78)7bc0c4f492fbceb1a67b81d09393b3d9$$aGrützmann, Konrad$$b5
000132912 7001_ $$aThürmann, Loreen$$b6
000132912 7001_ $$0P:(DE-He78)ba69542e8644b99720d1446ad757efa8$$aBauer, Tobias$$b7
000132912 7001_ $$0P:(DE-He78)4096eeffdfc73b75e8ba63dc621a017d$$aIshaque, Naveed$$b8
000132912 7001_ $$0P:(DE-He78)c954da35a243d177fdc4a3924f4f8a5c$$aSchick, Matthias$$b9
000132912 7001_ $$0P:(DE-He78)7999346780553d7fab7ba69d5afdfa71$$aBewerunge-Hudler, Melanie$$b10
000132912 7001_ $$aRöder, Stefan$$b11
000132912 7001_ $$aBauer, Mario$$b12
000132912 7001_ $$aSchulz, Angela$$b13
000132912 7001_ $$aBorte, Michael$$b14
000132912 7001_ $$aLandgraf, Kathrin$$b15
000132912 7001_ $$aKörner, Antje$$b16
000132912 7001_ $$aKiess, Wieland$$b17
000132912 7001_ $$avon Bergen, Martin$$b18
000132912 7001_ $$aStangl, Gabriele I$$b19
000132912 7001_ $$aTrump, Saskia$$b20
000132912 7001_ $$0P:(DE-He78)78b6aa82148e60b4d91e3a37a6d3d9a0$$aEils, Roland$$b21$$eLast author
000132912 7001_ $$aPolte, Tobias$$b22
000132912 7001_ $$aLehmann, Irina$$b23
000132912 773__ $$0PERI:(DE-600)2553921-8$$a10.1186/s13148-018-0478-z$$gVol. 10, no. 1, p. 58$$n1$$p58$$tClinical epigenetics$$v10$$x1868-7083$$y2018
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