Prenatal exposure to maternal depression, neonatal methylation of human glucocorticoid receptor gene (NR3C1) and infant cortisol stress responses. Oberlander, T. F, Weinberg, J., Papsdorf, M., Grunau, R., Misri, S., & Devlin, A. M Epigenetics : official journal of the DNA Methylation Society, 3(2):97–106, January, 2008.
Paper abstract bibtex 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. 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. 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. 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. 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.
@article{oberlander_prenatal_2008,
title = {Prenatal exposure to maternal depression, neonatal methylation of human glucocorticoid receptor gene ({NR3C1}) and infant cortisol stress responses.},
volume = {3},
issn = {1559-2308},
url = {http://www.ncbi.nlm.nih.gov/pubmed/18536531},
abstract = {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. 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. 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. 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. 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.},
number = {2},
urldate = {2015-05-26},
journal = {Epigenetics : official journal of the DNA Methylation Society},
author = {Oberlander, Tim F and Weinberg, Joanne and Papsdorf, Michael and Grunau, Ruth and Misri, Shaila and Devlin, Angela M},
month = jan,
year = {2008},
pmid = {18536531},
keywords = {Adult, Antidepressive Agents, Base Sequence, CpG Islands, DNA Methylation, Depression, Depression: drug therapy, Depression: genetics, Exons, Female, Fetal Blood, Fetal Blood: cytology, Fetal Blood: metabolism, Genetic, Glucocorticoid, Glucocorticoid: genetics, Humans, Hydrocortisone, Hydrocortisone: metabolism, Hypothalamo-Hypophyseal System, Infant, Leukocytes, Molecular Sequence Data, Mononuclear, Mononuclear: metabolism, Mothers, Mothers: psychology, Pituitary-Adrenal System, Pregnancy, Pregnancy Complications, Pregnancy Complications: genetics, Promoter Regions, Receptors, Second-Generation, Second-Generation: therapeu, Serotonin Uptake Inhibitors, Serotonin Uptake Inhibitors: therapeutic use},
pages = {97--106},
}
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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. 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. 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. 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.","number":"2","urldate":"2015-05-26","journal":"Epigenetics : official journal of the DNA Methylation Society","author":[{"propositions":[],"lastnames":["Oberlander"],"firstnames":["Tim","F"],"suffixes":[]},{"propositions":[],"lastnames":["Weinberg"],"firstnames":["Joanne"],"suffixes":[]},{"propositions":[],"lastnames":["Papsdorf"],"firstnames":["Michael"],"suffixes":[]},{"propositions":[],"lastnames":["Grunau"],"firstnames":["Ruth"],"suffixes":[]},{"propositions":[],"lastnames":["Misri"],"firstnames":["Shaila"],"suffixes":[]},{"propositions":[],"lastnames":["Devlin"],"firstnames":["Angela","M"],"suffixes":[]}],"month":"January","year":"2008","pmid":"18536531","keywords":"Adult, Antidepressive Agents, Base Sequence, CpG Islands, DNA Methylation, Depression, Depression: drug therapy, Depression: genetics, Exons, Female, Fetal Blood, Fetal Blood: cytology, Fetal Blood: metabolism, Genetic, Glucocorticoid, Glucocorticoid: genetics, Humans, Hydrocortisone, Hydrocortisone: metabolism, Hypothalamo-Hypophyseal System, Infant, Leukocytes, Molecular Sequence Data, Mononuclear, Mononuclear: metabolism, Mothers, Mothers: psychology, Pituitary-Adrenal System, Pregnancy, Pregnancy Complications, Pregnancy Complications: genetics, Promoter Regions, Receptors, Second-Generation, Second-Generation: therapeu, Serotonin Uptake Inhibitors, Serotonin Uptake Inhibitors: therapeutic use","pages":"97–106","bibtex":"@article{oberlander_prenatal_2008,\n\ttitle = {Prenatal exposure to maternal depression, neonatal methylation of human glucocorticoid receptor gene ({NR3C1}) and infant cortisol stress responses.},\n\tvolume = {3},\n\tissn = {1559-2308},\n\turl = {http://www.ncbi.nlm.nih.gov/pubmed/18536531},\n\tabstract = {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. 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. 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. 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. 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.},\n\tnumber = {2},\n\turldate = {2015-05-26},\n\tjournal = {Epigenetics : official journal of the DNA Methylation Society},\n\tauthor = {Oberlander, Tim F and Weinberg, Joanne and Papsdorf, Michael and Grunau, Ruth and Misri, Shaila and Devlin, Angela M},\n\tmonth = jan,\n\tyear = {2008},\n\tpmid = {18536531},\n\tkeywords = {Adult, Antidepressive Agents, Base Sequence, CpG Islands, DNA Methylation, Depression, Depression: drug therapy, Depression: genetics, Exons, Female, Fetal Blood, Fetal Blood: cytology, Fetal Blood: metabolism, Genetic, Glucocorticoid, Glucocorticoid: genetics, Humans, Hydrocortisone, Hydrocortisone: metabolism, Hypothalamo-Hypophyseal System, Infant, Leukocytes, Molecular Sequence Data, Mononuclear, Mononuclear: metabolism, Mothers, Mothers: psychology, Pituitary-Adrenal System, Pregnancy, Pregnancy Complications, Pregnancy Complications: genetics, Promoter Regions, Receptors, Second-Generation, Second-Generation: therapeu, Serotonin Uptake Inhibitors, Serotonin Uptake Inhibitors: therapeutic use},\n\tpages = {97--106},\n}\n\n","author_short":["Oberlander, T. 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