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 et/ou numérique 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 et/ou numérique] / 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 et/ou numérique 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 et/ou numérique] / 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 et/ou numérique 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 et/ou numérique] / 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

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 et/ou numérique 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 et/ou numérique] / 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)  

Public ISBD [article]  inAutism Research > 16-5 (May 2023) . - p.918-934 Titre : A multi-omic approach identifies an autism spectrum disorder (ASD) regulatory complex of functional epimutations in placentas from children born preterm Type de document : Texte imprimé et/ou numérique Auteurs : Anastasia N. FREEDMAN, Auteur ; Jeliyah CLARK, Auteur ; Lauren A. EAVES, Auteur ; Kyle ROELL, Auteur ; Ali ORAN, Auteur ; Lauren KOVAL, Auteur ; Julia RAGER, Auteur ; Hudson P. SANTOS JR., Auteur ; Karl KUBAN, Auteur ; Robert M. JOSEPH, Auteur ; Jean FRAZIER, Auteur ; Carmen J. MARSIT, Auteur ; Amber A. BURT, Auteur ; T. Michael O'SHEA, Auteur ; Rebecca C. FRY, Auteur Article en page(s) : p.918-934 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Abstract Children born preterm are at heightened risk of neurodevelopmental impairments, including Autism Spectrum Disorder (ASD). The placenta is a key regulator of neurodevelopmental processes, though the precise underlying molecular mechanisms remain unclear. Here, we employed a multi-omic approach to identify placental transcriptomic and epigenetic modifications related to ASD diagnosis at age 10, among children born preterm. Working with the extremely low gestational age (ELGAN) cohort, we hypothesized that a pro-inflammatory placental environment would be predictive of ASD diagnosis at age 10. Placental messenger RNA (mRNA) expression, CpG methylation, and microRNA (miRNA) expression were compared among 368 ELGANs (28 children diagnosed with ASD and 340 children without ASD). A total of 111 genes displayed expression levels in the placenta that were associated with ASD. Within these ASD-associated genes is an ASD regulatory complex comprising key genes that predicted ASD case status. Genes with expression that predicted ASD case status included Ewing Sarcoma Breakpoint Region 1 (EWSR1) (OR: 6.57 (95% CI: 2.34, 23.58)) and Bromodomain Adjacent To Zinc Finger Domain 2A (BAZ2A) (OR: 0.12 (95% CI: 0.03, 0.35)). Moreover, of the 111 ASD-associated genes, nine (8.1%) displayed associations with CpG methylation levels, while 14 (12.6%) displayed associations with miRNA expression levels. Among these, LRR Binding FLII Interacting Protein 1 (LRRFIP1) was identified as being under the control of both CpG methylation and miRNAs, displaying an OR of 0.42 (95% CI: 0.17, 0.95). This gene, as well as others identified as having functional epimutations, plays a critical role in immune system regulation and inflammatory response. In summary, a multi-omic approach was used to identify functional epimutations in the placenta that are associated with the development of ASD in children born preterm, highlighting future avenues for intervention. En ligne : http://dx.doi.org/https://doi.org/10.1002/aur.2915 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=503 [article] A multi-omic approach identifies an autism spectrum disorder (ASD) regulatory complex of functional epimutations in placentas from children born preterm [Texte imprimé et/ou numérique] / Anastasia N. FREEDMAN, Auteur ; Jeliyah CLARK, Auteur ; Lauren A. EAVES, Auteur ; Kyle ROELL, Auteur ; Ali ORAN, Auteur ; Lauren KOVAL, Auteur ; Julia RAGER, Auteur ; Hudson P. SANTOS JR., Auteur ; Karl KUBAN, Auteur ; Robert M. JOSEPH, Auteur ; Jean FRAZIER, Auteur ; Carmen J. MARSIT, Auteur ; Amber A. BURT, Auteur ; T. Michael O'SHEA, Auteur ; Rebecca C. FRY, Auteur . - p.918-934. Langues : Anglais (eng) in Autism Research > 16-5 (May 2023) . - p.918-934 Index. décimale : PER Périodiques Résumé : Abstract Children born preterm are at heightened risk of neurodevelopmental impairments, including Autism Spectrum Disorder (ASD). The placenta is a key regulator of neurodevelopmental processes, though the precise underlying molecular mechanisms remain unclear. Here, we employed a multi-omic approach to identify placental transcriptomic and epigenetic modifications related to ASD diagnosis at age 10, among children born preterm. Working with the extremely low gestational age (ELGAN) cohort, we hypothesized that a pro-inflammatory placental environment would be predictive of ASD diagnosis at age 10. Placental messenger RNA (mRNA) expression, CpG methylation, and microRNA (miRNA) expression were compared among 368 ELGANs (28 children diagnosed with ASD and 340 children without ASD). A total of 111 genes displayed expression levels in the placenta that were associated with ASD. Within these ASD-associated genes is an ASD regulatory complex comprising key genes that predicted ASD case status. Genes with expression that predicted ASD case status included Ewing Sarcoma Breakpoint Region 1 (EWSR1) (OR: 6.57 (95% CI: 2.34, 23.58)) and Bromodomain Adjacent To Zinc Finger Domain 2A (BAZ2A) (OR: 0.12 (95% CI: 0.03, 0.35)). Moreover, of the 111 ASD-associated genes, nine (8.1%) displayed associations with CpG methylation levels, while 14 (12.6%) displayed associations with miRNA expression levels. Among these, LRR Binding FLII Interacting Protein 1 (LRRFIP1) was identified as being under the control of both CpG methylation and miRNAs, displaying an OR of 0.42 (95% CI: 0.17, 0.95). This gene, as well as others identified as having functional epimutations, plays a critical role in immune system regulation and inflammatory response. In summary, a multi-omic approach was used to identify functional epimutations in the placenta that are associated with the development of ASD in children born preterm, highlighting future avenues for intervention. En ligne : http://dx.doi.org/https://doi.org/10.1002/aur.2915 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=503

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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