RESUMEN
BACKGROUND: Sex differences in the behaviour of children exposed to prenatal maternal depression and anxiety have been reported. This study compared depression and anxiety symptoms reported by mothers at term with maternal perceptions of one year old male and female infant temperament and with researcher observed infant characteristics, identifying differences for males and females with both approaches. METHODS: Infant behaviour and temperament was assessed via maternally completed questionnaires including Infant Behavioural Questionnaire Revised - Short form and by researcher administered subcomponents of Laboratory Temperament Assessment Battery and Bayley Scales of Infant Development III. RESULTS: For female infants, higher prenatal scores for depression and anxiety were associated with maternal perceptions of lower bonding, higher aggression and negativity, and lower soothability (nâ¯=â¯67 mother-infant dyads). In the laboratory assessment, intensity of escape was the only female infant factor significantly associated with maternal mood (nâ¯=â¯41). For male infants, there was minimal association between prenatal mood scores and maternal perceptions (nâ¯=â¯46) whereas in the laboratory assessment (nâ¯=â¯35) depression scores were associated with expressive language, facial interest and facial fear while anxiety scores were associated with expressive and receptive language, parent behaviour and facial fear. LIMITATIONS: Findings may be restricted to a single ethnicity or mode of delivery. Fewer infants attended the infant assessment. A laboratory setting may mask symptomatology in females. CONCLUSIONS: Atypical maternal perceptions may present a barrier to the early identification of male infants impacted by maternal depression and anxiety.
Asunto(s)
Ansiedad , Depresión , Relaciones Madre-Hijo , Temperamento , Ansiedad/epidemiología , Depresión/epidemiología , Femenino , Humanos , Lactante , Masculino , Madres , Percepción , Embarazo , Caracteres SexualesRESUMEN
INTRODUCTION: Telomeres, are composed of tandem repeat sequences located at the ends of chromosomes and are required to maintain genomic stability. Telomeres can become shorter due to cell division and specific lifestyle factors. Critically shortened telomeres are linked to cellular dysfunction, senescence and aging. A number of studies have used low resolution techniques to assess telomere length in the placenta. In this study, we applied Single Telomere Length Analysis (STELA) which provides high-resolution chromosome specific telomere length profiles to ask whether we could obtain more detailed information on the length of individual telomeres in the placenta. METHODS: Term placentas (37-42 weeks) were collected from women delivering at University Hospital of Wales or Royal Gwent Hospital within 2 h of delivery. Multiple telomere-length distributions were determined using STELA. Intraplacental variation of telomere length was analysed (N = 5). Telomere length distributions were compared between labouring (N = 10) and non-labouring (N = 11) participants. Finally, telomere length was compared between female (N = 17) and male (N = 20) placenta. RESULTS: There were no significant influences of sampling site, mode of delivery or foetal sex on the telomere-length distributions obtained. The mean telomere length was 7.7 kb ranging from 5.0 kb to 11.7 kb across all samples (N = 42) and longer compared with other human tissues at birth. STELA also revealed considerable telomere length heterogeneity within samples. CONCLUSIONS: We have shown that STELA can be used to study telomere length homeostasis in the placenta regardless of sampling site, mode of delivery and foetal sex. Moreover, as each amplicon is derived from a single telomeric molecule, from a single cell, STELA can reveal the full detail of telomere-length distributions, including telomeres within the length ranges observed in senescent cells. STELA thus provides a new tool to interrogate the relationship between telomere length and pregnancy complications linked to placental dysfunction.
Asunto(s)
Retardo del Crecimiento Fetal/metabolismo , Placenta/metabolismo , Homeostasis del Telómero , Adulto , Parto Obstétrico , Femenino , Humanos , Recién Nacido , Masculino , Embarazo , Caracteres Sexuales , Adulto JovenRESUMEN
BACKGROUND: Maternal prenatal stress during pregnancy is associated with fetal growth restriction and adverse neurodevelopmental outcomes, which may be mediated by impaired placental function. Imprinted genes control fetal growth, placental development, adult behaviour (including maternal behaviour) and placental lactogen production. This study examined whether maternal prenatal depression was associated with aberrant placental expression of the imprinted genes paternally expressed gene 3 (PEG3), paternally expressed gene 10 (PEG10), pleckstrin homology-like domain family a member 2 (PHLDA2) and cyclin-dependent kinase inhibitor 1C (CDKN1C), and resulting impaired placental human placental lactogen (hPL) expression. METHOD: A diagnosis of depression during pregnancy was recorded from Manchester cohort participants' medical notes (n = 75). Queen Charlotte's (n = 40) and My Baby and Me study (MBAM) (n = 81) cohort participants completed the Edinburgh Postnatal Depression Scale self-rating psychometric questionnaire. Villous trophoblast tissue samples were analysed for gene expression. RESULTS: In a pilot study, diagnosed depression during pregnancy was associated with a significant reduction in placental PEG3 expression (41%, p = 0.02). In two further independent cohorts, the Queen Charlotte's and MBAM cohorts, placental PEG3 expression was also inversely associated with maternal depression scores, an association that was significant in male but not female placentas. Finally, hPL expression was significantly decreased in women with clinically diagnosed depression (44%, p < 0.05) and in those with high depression scores (31% and 21%, respectively). CONCLUSIONS: This study provides the first evidence that maternal prenatal depression is associated with changes in the placental expression of PEG3, co-incident with decreased expression of hPL. This aberrant placental gene expression could provide a possible mechanistic explanation for the co-occurrence of maternal depression, fetal growth restriction, impaired maternal behaviour and poorer offspring outcomes.
Asunto(s)
Depresión/metabolismo , Expresión Génica/genética , Impresión Genómica/genética , Factores de Transcripción de Tipo Kruppel/metabolismo , Placenta/metabolismo , Complicaciones del Embarazo/metabolismo , Adulto , Estudios de Cohortes , Depresión/genética , Inglaterra , Femenino , Humanos , Lactógeno Placentario/metabolismo , Embarazo , Complicaciones del Embarazo/genética , Factores SexualesRESUMEN
Substantial data demonstrate that the early-life environment, including in utero, plays a key role in later life disease. In particular, maternal stress during pregnancy has been linked to adverse behavioural and emotional outcomes in children. Data from human cohort studies and experimental animal models suggest that modulation of the developing epigenome in the foetus by maternal stress may contribute to the foetal programming of disease. Here, we summarise insights gained from recent studies that may advance our understanding of the role of the placenta in mediating the association between maternal mood disorders and offspring outcomes. First, the placenta provides a record of exposures during pregnancy, as indicated by changes in the placental trancriptome and epigenome. Second, prenatal maternal mood may alter placental function to adversely impact foetal and child development. Finally, we discuss the less well established but interesting possibility that altered placental function, more specifically changes in placental hormones, may adversely affect maternal mood and later maternal behaviour, which can also have consequence for offspring well-being.
Asunto(s)
Afecto , Trastornos de la Conducta Infantil , Intercambio Materno-Fetal , Placenta/fisiología , Efectos Tardíos de la Exposición Prenatal , Estrés Psicológico , Animales , Niño , Epigénesis Genética , Femenino , Desarrollo Fetal , Humanos , Conducta Materna , Embarazo , Problema de ConductaRESUMEN
UNLABELLED: Imprinted genes, which are monoallelically expressed by virtue of an epigenetic process initiated in the germline, are known to play key roles in regulating fetal growth and placental development. Numerous studies are investigating the expression of these imprinted genes in the human placenta in relation to common complications of pregnancy such as fetal growth restriction and preeclampsia. This study aimed to determine whether placental sampling protocols or other factors such as fetal sex, gestational age and mode of delivery may influence the expression of imprinted genes predicted to regulate placental signalling. METHODS: Term placentas were collected from Caucasian women delivering at University Hospital of Wales or Royal Gwent Hospital within two hours of delivery. Expression of the imprinted genes PHLDA2, CDKN1C, PEG3 and PEG10 was assayed by quantitative real time PCR. Intraplacental gene expression was analysed (N = 5). Placental gene expression was compared between male (N = 11) and female (N = 11) infants, early term (N = 8) and late term (N = 10) deliveries and between labouring (N = 13) and non-labouring (N = 21) participants. RESULTS: The paternally expressed imprinted genes PEG3 and PEG10 were resilient to differences in sampling site, fetal sex, term gestational age and mode of delivery. The maternally expressed imprinted gene CDKN1C was elevated over 2-fold (p < 0.001) in placenta from labouring deliveries compared with elective caesarean sections. In addition, the maternally expressed imprinted gene PHLDA2 was elevated by 1.8 fold (p = 0.01) in samples taken at the distal edge of the placenta compared to the cord insertion site. CONCLUSION: These findings support the reinterpretation of existing data sets on these genes in relation to complications of pregnancy and further reinforce the importance of optimising and unifying placental collection protocols for future studies.