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. ![Prenatal exposure to maternal depression, neonatal methylation of human glucocorticoid receptor gene (NR3C1) and infant cortisol stress responses. [link]](https://bibbase.org/img/filetypes/link.svg "link")
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},
}
Downloads: 0
{"_id":"PuL5cSMQ8rJXNsqqs","bibbaseid":"oberlander-weinberg-papsdorf-grunau-misri-devlin-prenatalexposuretomaternaldepressionneonatalmethylationofhumanglucocorticoidreceptorgenenr3c1andinfantcortisolstressresponses-2008","author_short":["Oberlander, T. F","Weinberg, J.","Papsdorf, M.","Grunau, R.","Misri, S.","Devlin, A. M"],"bibdata":{"bibtype":"article","type":"article","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":[{"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. F","Weinberg, J.","Papsdorf, M.","Grunau, R.","Misri, S.","Devlin, A. M"],"key":"oberlander_prenatal_2008","id":"oberlander_prenatal_2008","bibbaseid":"oberlander-weinberg-papsdorf-grunau-misri-devlin-prenatalexposuretomaternaldepressionneonatalmethylationofhumanglucocorticoidreceptorgenenr3c1andinfantcortisolstressresponses-2008","role":"author","urls":{"Paper":"http://www.ncbi.nlm.nih.gov/pubmed/18536531"},"keyword":["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"],"metadata":{"authorlinks":{}},"html":""},"bibtype":"article","biburl":"https://bibbase.org/zotero/asrommel","dataSources":["J8fbWsdsy3xAaB3pX"],"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"],"search_terms":["prenatal","exposure","maternal","depression","neonatal","methylation","human","glucocorticoid","receptor","gene","nr3c1","infant","cortisol","stress","responses","oberlander","weinberg","papsdorf","grunau","misri","devlin"],"title":"Prenatal exposure to maternal depression, neonatal methylation of human glucocorticoid receptor gene (NR3C1) and infant cortisol stress responses.","year":2008}