Change in FK506 binding protein 5 (FKBP5) methylation over time among preschoolers with adversity / Stephanie H. PARADE in Development and Psychopathology, 29-5 (December 2017)  

Public ISBD [article]  inDevelopment and Psychopathology > 29-5 (December 2017) . - p.1627-1634 Titre : Change in FK506 binding protein 5 (FKBP5) methylation over time among preschoolers with adversity Type de document : texte imprimé Auteurs : Stephanie H. PARADE, Auteur ; Justin PARENT, Auteur ; Kantoniony RABEMANANJARA, Auteur ; Ronald SEIFER, Auteur ; Carmen J. MARSIT, Auteur ; Bao-Zhu YANG, Auteur ; Huiping ZHANG, Auteur ; Audrey R. TYRKA, Auteur Article en page(s) : p.1627-1634 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : FK506 binding protein 5 (FKBP5) alters stress response system functioning, and childhood maltreatment is associated with methylation of the FKBP5 gene. Yet it is unknown if maltreatment contributes to change in FKBP5 methylation over time. The current study draws upon a sample of 231 preschoolers, including 123 with child welfare documentation of moderate to severe maltreatment in the past 6 months, to understand if maltreatment contributes to change in FKBP5 methylation over a 6-month period. Review of child protection records and semistructured interviews in the home were used to assess maltreatment and exposure to other contextual stressors, as well as service utilization. Methylation of FKBP5 at two CpG sites in intron 7 was measured from saliva DNA at the time of initial study enrollment, and 6 months following enrollment. Child maltreatment was associated with change in FKBP5 methylation over time, but only when children were exposed to high levels of other contextual stressors. Service utilization was associated with increases in methylation over time, but only among children with the FKPB5 rs1360780 protective CC genotype. Methylation of FKBP5 is sensitive to stress exposure and may be a mechanism linking early adversity to long-term health and developmental outcomes. En ligne : http://dx.doi.org/10.1017/S0954579417001286 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=323 [article] Change in FK506 binding protein 5 (FKBP5) methylation over time among preschoolers with adversity [texte imprimé] / Stephanie H. PARADE, Auteur ; Justin PARENT, Auteur ; Kantoniony RABEMANANJARA, Auteur ; Ronald SEIFER, Auteur ; Carmen J. MARSIT, Auteur ; Bao-Zhu YANG, Auteur ; Huiping ZHANG, Auteur ; Audrey R. TYRKA, Auteur . - p.1627-1634. Langues : Anglais (eng) in Development and Psychopathology > 29-5 (December 2017) . - p.1627-1634 Index. décimale : PER Périodiques Résumé : FK506 binding protein 5 (FKBP5) alters stress response system functioning, and childhood maltreatment is associated with methylation of the FKBP5 gene. Yet it is unknown if maltreatment contributes to change in FKBP5 methylation over time. The current study draws upon a sample of 231 preschoolers, including 123 with child welfare documentation of moderate to severe maltreatment in the past 6 months, to understand if maltreatment contributes to change in FKBP5 methylation over a 6-month period. Review of child protection records and semistructured interviews in the home were used to assess maltreatment and exposure to other contextual stressors, as well as service utilization. Methylation of FKBP5 at two CpG sites in intron 7 was measured from saliva DNA at the time of initial study enrollment, and 6 months following enrollment. Child maltreatment was associated with change in FKBP5 methylation over time, but only when children were exposed to high levels of other contextual stressors. Service utilization was associated with increases in methylation over time, but only among children with the FKPB5 rs1360780 protective CC genotype. Methylation of FKBP5 is sensitive to stress exposure and may be a mechanism linking early adversity to long-term health and developmental outcomes. En ligne : http://dx.doi.org/10.1017/S0954579417001286 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=323

Childhood maltreatment and methylation of FK506 binding protein 5 gene (FKBP5) / Audrey R. TYRKA in Development and Psychopathology, 27-4 (Part 2) (November 2015)  

Public ISBD [article]  inDevelopment and Psychopathology > 27-4 (Part 2) (November 2015) . - p.1637-1645 Titre : Childhood maltreatment and methylation of FK506 binding protein 5 gene (FKBP5) Type de document : texte imprimé Auteurs : Audrey R. TYRKA, Auteur ; Kathryn K. RIDOUT, Auteur ; Stephanie H. PARADE, Auteur ; Alison PAQUETTE, Auteur ; Carmen J. MARSIT, Auteur ; Ronald SEIFER, Auteur Article en page(s) : p.1637-1645 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : A growing body of evidence suggests that alterations of the stress response system may be a mechanism by which childhood maltreatment alters risk for psychopathology. FK506 binding protein 51 (FKBP5) binds to the glucocorticoid receptor and alters its ability to respond to stress signaling. The aim of the present study was to examine methylation of the FKBP5 gene (FKBP5), and the role of an FKBP5 genetic variant, in relation to childhood maltreatment in a sample of impoverished preschool-aged children. One hundred seventy-four families participated in this study, including 69 with child welfare documentation of moderate to severe maltreatment in the past 6 months. The children, who ranged in age from 3 to 5 years, were racially and ethnically diverse. Structured record review and interviews in the home were used to assess a history of maltreatment, other traumas, and contextual life stressors; and a composite variable assessed the number exposures to these adversities. Methylation of two sites in intron 7 of FKBP5 was measured via sodium bisulfite pyrosequencing. Maltreated children had significantly lower levels of methylation at both CpG sites (p < .05). Lifetime contextual stress exposure showed a trend for lower levels of methylation at one of the sites, and a trend for an interaction with the FKBP5 polymorphism. A composite adversity variable was associated with lower levels of methylation at one of the sites as well (p < .05). FKBP5 alters glucocorticoid receptor responsiveness, and FKBP5 gene methylation may be a mechanism of the biobehavioral effects of adverse exposures in young children. En ligne : http://dx.doi.org/10.1017/S0954579415000991 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=273 [article] Childhood maltreatment and methylation of FK506 binding protein 5 gene (FKBP5) [texte imprimé] / Audrey R. TYRKA, Auteur ; Kathryn K. RIDOUT, Auteur ; Stephanie H. PARADE, Auteur ; Alison PAQUETTE, Auteur ; Carmen J. MARSIT, Auteur ; Ronald SEIFER, Auteur . - p.1637-1645. Langues : Anglais (eng) in Development and Psychopathology > 27-4 (Part 2) (November 2015) . - p.1637-1645 Index. décimale : PER Périodiques Résumé : A growing body of evidence suggests that alterations of the stress response system may be a mechanism by which childhood maltreatment alters risk for psychopathology. FK506 binding protein 51 (FKBP5) binds to the glucocorticoid receptor and alters its ability to respond to stress signaling. The aim of the present study was to examine methylation of the FKBP5 gene (FKBP5), and the role of an FKBP5 genetic variant, in relation to childhood maltreatment in a sample of impoverished preschool-aged children. One hundred seventy-four families participated in this study, including 69 with child welfare documentation of moderate to severe maltreatment in the past 6 months. The children, who ranged in age from 3 to 5 years, were racially and ethnically diverse. Structured record review and interviews in the home were used to assess a history of maltreatment, other traumas, and contextual life stressors; and a composite variable assessed the number exposures to these adversities. Methylation of two sites in intron 7 of FKBP5 was measured via sodium bisulfite pyrosequencing. Maltreated children had significantly lower levels of methylation at both CpG sites (p < .05). Lifetime contextual stress exposure showed a trend for lower levels of methylation at one of the sites, and a trend for an interaction with the FKBP5 polymorphism. A composite adversity variable was associated with lower levels of methylation at one of the sites as well (p < .05). FKBP5 alters glucocorticoid receptor responsiveness, and FKBP5 gene methylation may be a mechanism of the biobehavioral effects of adverse exposures in young children. En ligne : http://dx.doi.org/10.1017/S0954579415000991 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=273

Dynamic stress-related epigenetic regulation of the glucocorticoid receptor gene promoter during early development: The role of child maltreatment / Justin PARENT in Development and Psychopathology, 29-5 (December 2017)  

Public ISBD [article]  inDevelopment and Psychopathology > 29-5 (December 2017) . - p.1635-1648 Titre : Dynamic stress-related epigenetic regulation of the glucocorticoid receptor gene promoter during early development: The role of child maltreatment Type de document : texte imprimé Auteurs : Justin PARENT, Auteur ; Stephanie H. PARADE, Auteur ; Laura E. LAUMANN, Auteur ; Kathryn K. RIDOUT, Auteur ; Bao-Zhu YANG, Auteur ; Carmen J. MARSIT, Auteur ; Ronald SEIFER, Auteur ; Audrey R. TYRKA, Auteur Article en page(s) : p.1635-1648 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Epigenetics processes may play a vital role in the biological embedding of early environmental adversity and the development of psychopathology. Accumulating evidence suggests that maltreatment is linked to methylation of the glucocorticoid receptor gene, nuclear receptor subfamily 3, group C, member 1 (NR3C1), which is a key regulator of the hypothalamus–pituitary–adrenal axis. However, prior work has been exclusively cross-sectional, greatly constraining our understanding of stress-related epigenetic processes over time. In the current study, we examined the effect of maltreatment and other adversity on change in NR3C1 methylation among at-risk preschoolers to begin to characterize within-child epigenetic changes during this sensitive developmental period. Participants were 260 preschoolers (3–5 years old, 53.8% female), including 51.5% with moderate to severe maltreatment in the past 6 months. Child protection records, semistructured interviews, and parent reports were used to assess child stress exposure. Methylation of exons 1D and 1F of NR3C1 via saliva DNA were measured at two time points approximately 6 months apart. Results indicate that maltreated children evidence higher baseline levels of NR3C1 methylation, significant decreases in methylation over time, and then at follow-up, lower levels of methylation, relative to nonmaltreated preschoolers. Findings from the current study highlight the complex nature of stress-related epigenetic processes during early development. En ligne : http://dx.doi.org/10.1017/S0954579417001298 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=323 [article] Dynamic stress-related epigenetic regulation of the glucocorticoid receptor gene promoter during early development: The role of child maltreatment [texte imprimé] / Justin PARENT, Auteur ; Stephanie H. PARADE, Auteur ; Laura E. LAUMANN, Auteur ; Kathryn K. RIDOUT, Auteur ; Bao-Zhu YANG, Auteur ; Carmen J. MARSIT, Auteur ; Ronald SEIFER, Auteur ; Audrey R. TYRKA, Auteur . - p.1635-1648. Langues : Anglais (eng) in Development and Psychopathology > 29-5 (December 2017) . - p.1635-1648 Index. décimale : PER Périodiques Résumé : Epigenetics processes may play a vital role in the biological embedding of early environmental adversity and the development of psychopathology. Accumulating evidence suggests that maltreatment is linked to methylation of the glucocorticoid receptor gene, nuclear receptor subfamily 3, group C, member 1 (NR3C1), which is a key regulator of the hypothalamus–pituitary–adrenal axis. However, prior work has been exclusively cross-sectional, greatly constraining our understanding of stress-related epigenetic processes over time. In the current study, we examined the effect of maltreatment and other adversity on change in NR3C1 methylation among at-risk preschoolers to begin to characterize within-child epigenetic changes during this sensitive developmental period. Participants were 260 preschoolers (3–5 years old, 53.8% female), including 51.5% with moderate to severe maltreatment in the past 6 months. Child protection records, semistructured interviews, and parent reports were used to assess child stress exposure. Methylation of exons 1D and 1F of NR3C1 via saliva DNA were measured at two time points approximately 6 months apart. Results indicate that maltreated children evidence higher baseline levels of NR3C1 methylation, significant decreases in methylation over time, and then at follow-up, lower levels of methylation, relative to nonmaltreated preschoolers. Findings from the current study highlight the complex nature of stress-related epigenetic processes during early development. En ligne : http://dx.doi.org/10.1017/S0954579417001298 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=323

Evidence for the placenta-brain axis: multi-omic kernel aggregation predicts intellectual and social impairment in children born extremely preterm / Hudson P. Jr SANTOS in Molecular Autism, 11 (2020)  

Public ISBD [article]  inMolecular Autism > 11 (2020) Titre : Evidence for the placenta-brain axis: multi-omic kernel aggregation predicts intellectual and social impairment in children born extremely preterm Type de document : texte imprimé Auteurs : Hudson P. Jr SANTOS, Auteur ; Arjun BHATTACHARYA, Auteur ; Robert M. JOSEPH, Auteur ; Lisa SMEESTER, Auteur ; Karl C.K. KUBAN, Auteur ; Carmen J. MARSIT, Auteur ; T. Michael O'SHEA, Auteur ; Rebecca C. FRY, Auteur Langues : Anglais (eng) Mots-clés : Differential expression analysis  Epigenome-wide association  Multi-omic aggregation  Placental gene regulation  Prenatal neurodevelopmental programming  Social and cognitive impairment Index. décimale : PER Périodiques Résumé : BACKGROUND: Children born extremely preterm are at heightened risk for intellectual and social impairment, including Autism Spectrum Disorder (ASD). There is increasing evidence for a key role of the placenta in prenatal developmental programming, suggesting that the placenta may, in part, contribute to origins of neurodevelopmental outcomes. METHODS: We examined associations between placental transcriptomic and epigenomic profiles and assessed their ability to predict intellectual and social impairment at age 10 years in 379 children from the Extremely Low Gestational Age Newborn (ELGAN) cohort. Assessment of intellectual ability (IQ) and social function was completed with the Differential Ability Scales-II and Social Responsiveness Scale (SRS), respectively. Examining IQ and SRS allows for studying ASD risk beyond the diagnostic criteria, as IQ and SRS are continuous measures strongly correlated with ASD. Genome-wide mRNA, CpG methylation and miRNA were assayeds with the Illumina Hiseq 2500, HTG EdgeSeq miRNA Whole Transcriptome Assay, and Illumina EPIC/850 K array, respectively. We conducted genome-wide differential analyses of placental mRNA, miRNA, and CpG methylation data. These molecular features were then integrated for a predictive analysis of IQ and SRS outcomes using kernel aggregation regression. We lastly examined associations between ASD and the multi-omic-predicted component of IQ and SRS. RESULTS: Genes with important roles in neurodevelopment and placental tissue organization were associated with intellectual and social impairment. Kernel aggregations of placental multi-omics strongly predicted intellectual and social function, explaining approximately 8% and 12% of variance in SRS and IQ scores via cross-validation, respectively. Predicted in-sample SRS and IQ showed significant positive and negative associations with ASD case-control status. LIMITATIONS: The ELGAN cohort comprises children born pre-term, and generalization may be affected by unmeasured confounders associated with low gestational age. We conducted external validation of predictive models, though the sample size (N = 49) and the scope of the available out-sample placental dataset are limited. Further validation of the models is merited. CONCLUSIONS: Aggregating information from biomarkers within and among molecular data types improves prediction of complex traits like social and intellectual ability in children born extremely preterm, suggesting that traits within the placenta-brain axis may be omnigenic. En ligne : http://dx.doi.org/10.1186/s13229-020-00402-w Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=438 [article] Evidence for the placenta-brain axis: multi-omic kernel aggregation predicts intellectual and social impairment in children born extremely preterm [texte imprimé] / Hudson P. Jr SANTOS, Auteur ; Arjun BHATTACHARYA, Auteur ; Robert M. JOSEPH, Auteur ; Lisa SMEESTER, Auteur ; Karl C.K. KUBAN, Auteur ; Carmen J. MARSIT, Auteur ; T. Michael O'SHEA, Auteur ; Rebecca C. FRY, Auteur. Langues : Anglais (eng) in Molecular Autism > 11 (2020) Mots-clés : Differential expression analysis  Epigenome-wide association  Multi-omic aggregation  Placental gene regulation  Prenatal neurodevelopmental programming  Social and cognitive impairment Index. décimale : PER Périodiques Résumé : BACKGROUND: Children born extremely preterm are at heightened risk for intellectual and social impairment, including Autism Spectrum Disorder (ASD). There is increasing evidence for a key role of the placenta in prenatal developmental programming, suggesting that the placenta may, in part, contribute to origins of neurodevelopmental outcomes. METHODS: We examined associations between placental transcriptomic and epigenomic profiles and assessed their ability to predict intellectual and social impairment at age 10 years in 379 children from the Extremely Low Gestational Age Newborn (ELGAN) cohort. Assessment of intellectual ability (IQ) and social function was completed with the Differential Ability Scales-II and Social Responsiveness Scale (SRS), respectively. Examining IQ and SRS allows for studying ASD risk beyond the diagnostic criteria, as IQ and SRS are continuous measures strongly correlated with ASD. Genome-wide mRNA, CpG methylation and miRNA were assayeds with the Illumina Hiseq 2500, HTG EdgeSeq miRNA Whole Transcriptome Assay, and Illumina EPIC/850 K array, respectively. We conducted genome-wide differential analyses of placental mRNA, miRNA, and CpG methylation data. These molecular features were then integrated for a predictive analysis of IQ and SRS outcomes using kernel aggregation regression. We lastly examined associations between ASD and the multi-omic-predicted component of IQ and SRS. RESULTS: Genes with important roles in neurodevelopment and placental tissue organization were associated with intellectual and social impairment. Kernel aggregations of placental multi-omics strongly predicted intellectual and social function, explaining approximately 8% and 12% of variance in SRS and IQ scores via cross-validation, respectively. Predicted in-sample SRS and IQ showed significant positive and negative associations with ASD case-control status. LIMITATIONS: The ELGAN cohort comprises children born pre-term, and generalization may be affected by unmeasured confounders associated with low gestational age. We conducted external validation of predictive models, though the sample size (N = 49) and the scope of the available out-sample placental dataset are limited. Further validation of the models is merited. CONCLUSIONS: Aggregating information from biomarkers within and among molecular data types improves prediction of complex traits like social and intellectual ability in children born extremely preterm, suggesting that traits within the placenta-brain axis may be omnigenic. En ligne : http://dx.doi.org/10.1186/s13229-020-00402-w Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=438

Methylation of exons 1D, 1F, and 1H of the glucocorticoid receptor gene promoter and exposure to adversity in preschool-aged children / Audrey R. TYRKA in Development and Psychopathology, 27-2 (May 2015)  

Public ISBD [article]  inDevelopment and Psychopathology > 27-2 (May 2015) . - p.577-585 Titre : Methylation of exons 1D, 1F, and 1H of the glucocorticoid receptor gene promoter and exposure to adversity in preschool-aged children Type de document : texte imprimé Auteurs : Audrey R. TYRKA, Auteur ; Stephanie H. PARADE, Auteur ; Nicole M. ESLINGER, Auteur ; Carmen J. MARSIT, Auteur ; Corina LESSEUR, Auteur ; David A. ARMSTRONG, Auteur ; Noah S. PHILIP, Auteur ; Brittney JOSEFSON, Auteur ; Ronald SEIFER, Auteur Article en page(s) : p.577-585 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Epigenetic modifications to the genome are a key mechanism involved in the biological encoding of experience. Animal studies and a growing body of literature in humans have shown that early adversity is linked to methylation of the gene for the glucocorticoid receptor (GR), which is a key regulator of the hypothalamic–pituitary–adrenal axis as well as a broad range of physiological systems including metabolic and immune function. One hundred eighty-four families participated, including n = 74 with child welfare documentation of moderate-severe maltreatment in the past 6 months. Children ranged in age from 3 to 5 years, and were racially and ethnically diverse. Structured record review and interviews in the home were used to assess a history of maltreatment, other traumas, and contextual life stressors, and a composite variable assessed the number exposures to these adversities. Methylation of regions 1D, 1F, and 1H of the GR gene was measured via sodium bisulfite pyrosequencing. The composite measure of adversity was positively correlated with methylation at exons 1D and 1F in the promoter of the GR gene. Individual stress measures were significantly associated with a several CpG sites in these regions. GR gene methylation may be a mechanism of the biobehavioral effects of adverse exposures in young children. En ligne : http://dx.doi.org/10.1017/S0954579415000176 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=257 [article] Methylation of exons 1D, 1F, and 1H of the glucocorticoid receptor gene promoter and exposure to adversity in preschool-aged children [texte imprimé] / Audrey R. TYRKA, Auteur ; Stephanie H. PARADE, Auteur ; Nicole M. ESLINGER, Auteur ; Carmen J. MARSIT, Auteur ; Corina LESSEUR, Auteur ; David A. ARMSTRONG, Auteur ; Noah S. PHILIP, Auteur ; Brittney JOSEFSON, Auteur ; Ronald SEIFER, Auteur . - p.577-585. Langues : Anglais (eng) in Development and Psychopathology > 27-2 (May 2015) . - p.577-585 Index. décimale : PER Périodiques Résumé : Epigenetic modifications to the genome are a key mechanism involved in the biological encoding of experience. Animal studies and a growing body of literature in humans have shown that early adversity is linked to methylation of the gene for the glucocorticoid receptor (GR), which is a key regulator of the hypothalamic–pituitary–adrenal axis as well as a broad range of physiological systems including metabolic and immune function. One hundred eighty-four families participated, including n = 74 with child welfare documentation of moderate-severe maltreatment in the past 6 months. Children ranged in age from 3 to 5 years, and were racially and ethnically diverse. Structured record review and interviews in the home were used to assess a history of maltreatment, other traumas, and contextual life stressors, and a composite variable assessed the number exposures to these adversities. Methylation of regions 1D, 1F, and 1H of the GR gene was measured via sodium bisulfite pyrosequencing. The composite measure of adversity was positively correlated with methylation at exons 1D and 1F in the promoter of the GR gene. Individual stress measures were significantly associated with a several CpG sites in these regions. GR gene methylation may be a mechanism of the biobehavioral effects of adverse exposures in young children. En ligne : http://dx.doi.org/10.1017/S0954579415000176 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=257

A multi-omic approach identifies an autism spectrum disorder (ASD) regulatory complex of functional epimutations in placentas from children born preterm / Anastasia N. FREEDMAN in Autism Research, 16-5 (May 2023)  

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Stress exposure and psychopathology alter methylation of the serotonin receptor 2A (HTR2A) gene in preschoolers / Stephanie H. PARADE in Development and Psychopathology, 29-5 (December 2017)  

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Trajectories of attention problems in preschoolers born very preterm / Francisco Xavier CASTELLANOS ; Brian S. CARTER ; Jennifer CHECK ; Jennifer HELDERMAN ; Julie A. HOFHEIMER ; Elisabeth C. MCGOWAN ; Charles R. NEAL ; Steven L. PASTYRNAK ; Lynne M. SMITH ; T. Michael O'SHEA ; Carmen J. MARSIT ; Barry M. LESTER in Journal of Child Psychology and Psychiatry, 66-5 (May 2025)  

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