<?xml version="1.0" encoding="UTF-8"?><xml><records><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Oberlander, Tim F</style></author><author><style face="normal" font="default" size="100%">Weinberg, Joanne</style></author><author><style face="normal" font="default" size="100%">Papsdorf, Michael</style></author><author><style face="normal" font="default" size="100%">Grunau, Ruth</style></author><author><style face="normal" font="default" size="100%">Misri, Shaila</style></author><author><style face="normal" font="default" size="100%">Devlin, Angela M</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Prenatal exposure to maternal depression, neonatal methylation of human glucocorticoid receptor gene (NR3C1) and infant cortisol stress responses.</style></title><secondary-title><style face="normal" font="default" size="100%">Epigenetics</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Epigenetics</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Adult</style></keyword><keyword><style  face="normal" font="default" size="100%">Antidepressive Agents, Second-Generation</style></keyword><keyword><style  face="normal" font="default" size="100%">Base Sequence</style></keyword><keyword><style  face="normal" font="default" size="100%">CpG Islands</style></keyword><keyword><style  face="normal" font="default" size="100%">Depression</style></keyword><keyword><style  face="normal" font="default" size="100%">DNA Methylation</style></keyword><keyword><style  face="normal" font="default" size="100%">Exons</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Fetal Blood</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Hydrocortisone</style></keyword><keyword><style  face="normal" font="default" size="100%">Hypothalamo-Hypophyseal System</style></keyword><keyword><style  face="normal" font="default" size="100%">Infant</style></keyword><keyword><style  face="normal" font="default" size="100%">Leukocytes, Mononuclear</style></keyword><keyword><style  face="normal" font="default" size="100%">Molecular Sequence Data</style></keyword><keyword><style  face="normal" font="default" size="100%">Mothers</style></keyword><keyword><style  face="normal" font="default" size="100%">Pituitary-Adrenal System</style></keyword><keyword><style  face="normal" font="default" size="100%">Pregnancy</style></keyword><keyword><style  face="normal" font="default" size="100%">Pregnancy Complications</style></keyword><keyword><style  face="normal" font="default" size="100%">Promoter Regions, Genetic</style></keyword><keyword><style  face="normal" font="default" size="100%">Receptors, Glucocorticoid</style></keyword><keyword><style  face="normal" font="default" size="100%">Serotonin Uptake Inhibitors</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2008</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2008 Mar-Apr</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">3</style></volume><pages><style face="normal" font="default" size="100%">97-106</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;BACKGROUND: In animal models, variations in early maternal care are associated with differences in hypothalamic-pituitary-adrenal(HPA) stress response in the offspring, mediated via changes in the epigenetic regulation of glucocorticoid receptor (GR) gene (Nr3c1) expression.&lt;/p&gt;
&lt;p&gt;OBJECTIVE: To study this in humans, relationships between prenatal exposure to maternal mood and the methylation status of a CpG-rich region in the promoter and exon 1F of the human GR gene (NR3C1) in newborns and HPA stress reactivity at age three months were examined.&lt;/p&gt;
&lt;p&gt;RESULTS: Prenatal exposure to increased third trimester maternal depressed/anxious mood was associated with increased methylation of NR3C1 at a predicted NGFI-A binding site. Increased NR3C1 methylation at this site was also associated with increased salivary cortisol stress responses at 3 months, controlling for prenatal SRI exposure, postnatal age and pre and postnatal maternal mood.&lt;/p&gt;
&lt;p&gt;METHODS: The methylation status of a CpG-rich region of the NR3C1 gene, including exon 1F, in genomic DNA from cord blood mononuclear cells was quantified by bisulfite pyrosequencing in infants of depressed mothers treated with a serotonin reuptake inhibitor antidepressant (SRI) (n = 33), infants of depressed nontreated mothers (n = 13) and infants of non depressed/non treated mothers (n = 36). To study the functional implications of the newborn methylation status of NR3C1 in newborns, HPA function was assessed at three months using salivary cortisol obtained before and following a non noxious stressor and at a late afternoon basal time.&lt;/p&gt;
&lt;p&gt;CONCLUSIONS: Methylation status of the human NR3C1 gene in newborns is sensitive to prenatal maternal mood and may offer a potential epigenetic process that links antenatal maternal mood and altered HPA stress reactivity during infancy.&lt;/p&gt;
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