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@ARTICLE{Junge:132912,
      author       = {K. M. Junge and B. Leppert and S. Jahreis and D. K.
                      Wissenbach and R. Feltens and K. Grützmann$^*$ and L.
                      Thürmann and T. Bauer$^*$ and N. Ishaque$^*$ and M.
                      Schick$^*$ and M. Bewerunge-Hudler$^*$ and S. Röder and M.
                      Bauer and A. Schulz and M. Borte and K. Landgraf and A.
                      Körner and W. Kiess and M. von Bergen and G. I. Stangl and
                      S. Trump and R. Eils$^*$ and T. Polte and I. Lehmann},
      title        = {{MEST} mediates the impact of prenatal bisphenol {A}
                      exposure on long-term body weight development.},
      journal      = {Clinical epigenetics},
      volume       = {10},
      number       = {1},
      issn         = {1868-7083},
      address      = {[S.l.]},
      publisher    = {BioMed Central},
      reportid     = {DKFZ-2018-00554},
      pages        = {58},
      year         = {2018},
      abstract     = {Exposure 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.},
      cin          = {L301 / B080 / W110},
      ddc          = {610},
      cid          = {I:(DE-He78)L301-20160331 / I:(DE-He78)B080-20160331 /
                      I:(DE-He78)W110-20160331},
      pnm          = {312 - Functional and structural genomics (POF3-312)},
      pid          = {G:(DE-HGF)POF3-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:29721103},
      pmc          = {pmc:PMC5910578},
      doi          = {10.1186/s13148-018-0478-z},
      url          = {https://inrepo02.dkfz.de/record/132912},
}