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Auteur Jennifer KRIEBEL |
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Associations of prenatal depressive symptoms with DNA methylation of HPA axis-related genes and diurnal cortisol profiles in primary school-aged children / Valeska STONAWSKI in Development and Psychopathology, 31-2 (May 2019)
[article]
Titre : Associations of prenatal depressive symptoms with DNA methylation of HPA axis-related genes and diurnal cortisol profiles in primary school-aged children Type de document : Texte imprimé et/ou numérique Auteurs : Valeska STONAWSKI, Auteur ; Stefan FREY, Auteur ; Yulia GOLUB, Auteur ; Nicolas ROHLEDER, Auteur ; Jennifer KRIEBEL, Auteur ; Tamme W. GOECKE, Auteur ; Peter A. FASCHING, Auteur ; Matthias W. BECKMANN, Auteur ; Johannes KORNHUBER, Auteur ; Oliver KRATZ, Auteur ; Gunther H. MOLL, Auteur ; Hartmut HEINRICH, Auteur ; Anna EICHLER, Auteur Article en page(s) : p.419-431 Langues : Anglais (eng) Mots-clés : cortisol DNA methylation epigenetics pregnancy prenatal depression Index. décimale : PER Périodiques Résumé : Epigenetic DNA modifications in genes related to the hypothalamic–pituitary–adrenal (HPA) axis are discussed as a mechanism underlying the association between prenatal depression and altered child HPA activity. In a longitudinal study, DNA methylation changes related to prenatal depressive symptoms were investigated in 167 children aged 6 to 9 years. At six candidate genes, 126 cytosine–guanine dinucleotides were considered without correcting for multiple testing due to the exploratory nature of the study. Further associations with the basal child HPA activity were examined. Children exposed to prenatal depressive symptoms exhibited lower bedtime cortisol (p = .003, ?p2 = 0.07) and a steeper diurnal slope (p = .023, ?p2 = 0.06). For total cortisol release, prenatal exposure was related to lower cortisol release in boys, and higher release in girls. Furthermore, prenatal depressive symptoms were associated with altered methylation in the glucocorticoid receptor gene (NR3C1), the mineralocorticoid receptor gene (NR3C2), and the serotonin receptor gene (SLC6A4), with some sex-specific effects (p = .012–.040, ?p2 = 0.03–0.04). In boys, prenatal depressive symptoms predicted bedtime cortisol mediated by NR3C2 methylation, indirect effect = –0.07, 95% confidence interval [–0.16, –0.02]. Results indicate relations of prenatal depressive symptoms to both child basal HPA activity and DNA methylation, partially fitting a mediation model, with exposed boys and girls being affected differently. En ligne : http://dx.doi.org/10.1017/S0954579418000056 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=393
in Development and Psychopathology > 31-2 (May 2019) . - p.419-431[article] Associations of prenatal depressive symptoms with DNA methylation of HPA axis-related genes and diurnal cortisol profiles in primary school-aged children [Texte imprimé et/ou numérique] / Valeska STONAWSKI, Auteur ; Stefan FREY, Auteur ; Yulia GOLUB, Auteur ; Nicolas ROHLEDER, Auteur ; Jennifer KRIEBEL, Auteur ; Tamme W. GOECKE, Auteur ; Peter A. FASCHING, Auteur ; Matthias W. BECKMANN, Auteur ; Johannes KORNHUBER, Auteur ; Oliver KRATZ, Auteur ; Gunther H. MOLL, Auteur ; Hartmut HEINRICH, Auteur ; Anna EICHLER, Auteur . - p.419-431.
Langues : Anglais (eng)
in Development and Psychopathology > 31-2 (May 2019) . - p.419-431
Mots-clés : cortisol DNA methylation epigenetics pregnancy prenatal depression Index. décimale : PER Périodiques Résumé : Epigenetic DNA modifications in genes related to the hypothalamic–pituitary–adrenal (HPA) axis are discussed as a mechanism underlying the association between prenatal depression and altered child HPA activity. In a longitudinal study, DNA methylation changes related to prenatal depressive symptoms were investigated in 167 children aged 6 to 9 years. At six candidate genes, 126 cytosine–guanine dinucleotides were considered without correcting for multiple testing due to the exploratory nature of the study. Further associations with the basal child HPA activity were examined. Children exposed to prenatal depressive symptoms exhibited lower bedtime cortisol (p = .003, ?p2 = 0.07) and a steeper diurnal slope (p = .023, ?p2 = 0.06). For total cortisol release, prenatal exposure was related to lower cortisol release in boys, and higher release in girls. Furthermore, prenatal depressive symptoms were associated with altered methylation in the glucocorticoid receptor gene (NR3C1), the mineralocorticoid receptor gene (NR3C2), and the serotonin receptor gene (SLC6A4), with some sex-specific effects (p = .012–.040, ?p2 = 0.03–0.04). In boys, prenatal depressive symptoms predicted bedtime cortisol mediated by NR3C2 methylation, indirect effect = –0.07, 95% confidence interval [–0.16, –0.02]. Results indicate relations of prenatal depressive symptoms to both child basal HPA activity and DNA methylation, partially fitting a mediation model, with exposed boys and girls being affected differently. En ligne : http://dx.doi.org/10.1017/S0954579418000056 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=393