scholarly journals Prenatal lead exposure and cord blood DNA methylation in PROGRESS: an epigenome-wide association study

2020 ◽  
Vol 6 (1) ◽  
Author(s):  
Jonathan A Heiss ◽  
Martha M Téllez-Rojo ◽  
Guadalupe Estrada-Gutiérrez ◽  
Lourdes Schnaas ◽  
Chitra Amarasiriwardena ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Cord Blood ◽  
Gestational Age ◽  
Lead Exposure ◽  
Inductively Coupled Plasma ◽  
Maternal Education ◽  
Association Studies ◽  
Mode Of Delivery ◽  
Underlying Mechanisms ◽  
Prenatal Lead Exposure

Abstract The effects of prenatal lead exposure on child development include impaired growth and cognitive function. DNA methylation might be involved in the underlying mechanisms and previous epigenome-wide association studies reported associations between lead exposure during pregnancy and cord blood methylation levels. However, it is unclear during which developmental stage lead exposure is most harmful. Cord blood methylation levels were assayed in 420 children from a Mexican pre-birth cohort using the Illumina Infinium MethylationEPIC microarray. Lead concentrations were measured in umbilical cord blood as well as in blood samples from the mothers collected at 2nd and 3rd trimester and delivery using inductively coupled plasma-mass spectrometry. In addition, maternal bone lead levels were measured in tibia and patella using X-ray fluorescence. Comprehensive quality control and preprocessing of microarray data was followed by an unbiased restriction to methylation sites with substantial variance. Methylation levels at 202 111 cytosine-phosphate-guanine sites were regressed on each exposure adjusting for child sex, leukocyte composition, batch variables, gestational age, birthweight-for-gestational-age, maternal age, maternal education and mode of delivery. We find no association between prenatal lead exposure and cord blood methylation. This null result is strengthened by a sensitivity analysis showing that in the same dataset known biomarkers for birthweight-for-gestational-age can be recovered and the fact that phenotypic associations with lead exposure have been described in the same cohort.

scholarly journals Prenatal lead exposure, telomere length in cord blood and DNA methylation age in the PROGRESS cohort

2021 ◽  
Vol 2021 (1) ◽  
Author(s):  
Jose Francisco Herrera Moreno ◽  
Haotian Wu ◽  
Tessa R. Bloomquist ◽  
Maria José Rosa ◽  
Allan C. Just ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Cord Blood ◽  
Telomere Length ◽  
Lead Exposure ◽  
Dna Methylation Age ◽  
Prenatal Lead Exposure

An Epigenome-Wide Association Study for Prenatal Lead Exposure and Umbilical Cord Blood DNA Methylation in Project Viva

2018 ◽  
Vol 2017 (1) ◽  
pp. 129
Author(s):  
Shaowei Wu ◽  
Marie-France Hivert ◽  
Andres Cardenas ◽  
Jia Zhong ◽  
Sheryl L. Rifas-Shiman ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Cord Blood ◽  
Association Study ◽  
Umbilical Cord ◽  
Umbilical Cord Blood ◽  
Lead Exposure ◽  
Prenatal Lead Exposure

Prenatal lead exposure, telomere length in cord blood, and DNA methylation age in the PROGRESS prenatal cohort

2021 ◽  
pp. 112577
Author(s):  
José F. Herrera-Moreno ◽  
Guadalupe Estrada-Gutierrez ◽  
Haotian Wu ◽  
Tessa R. Bloomquist ◽  
Maria José Rosa ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Cord Blood ◽  
Telomere Length ◽  
Lead Exposure ◽  
Dna Methylation Age ◽  
Prenatal Lead Exposure

Prenatal lead exposure and cord blood DNA methylation in the Korean Exposome Study

2021 ◽  
Vol 195 ◽  
pp. 110767
Author(s):  
Jaehyun Park ◽  
Jeeyoung Kim ◽  
Esther Kim ◽  
Woo Jin Kim ◽  
Sungho Won
Keyword(s):  
Dna Methylation ◽  
Cord Blood ◽  
Lead Exposure ◽  
Prenatal Lead Exposure

scholarly journals Birthweight DNA methylation signatures in infant saliva

2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Chiara Moccia ◽  
Maja Popovic ◽  
Elena Isaevska ◽  
Valentina Fiano ◽  
Morena Trevisan ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Cord Blood ◽  
Gestational Age ◽  
Low Birthweight ◽  
Continuous Variable ◽  
Linear Regression Models ◽  
Association Analyses ◽  
Cpg Sites ◽  
Adverse Health Outcomes ◽  
The Look

Abstract Background Low birthweight has been repeatedly associated with long-term adverse health outcomes and many non-communicable diseases. Our aim was to look-up cord blood birthweight-associated CpG sites identified by the PACE Consortium in infant saliva, and to explore saliva-specific DNA methylation signatures of birthweight. Methods DNA methylation was assessed using Infinium HumanMethylation450K array in 135 saliva samples collected from children of the NINFEA birth cohort at an average age of 10.8 (range 7–17) months. The association analyses between birthweight and DNA methylation variations were carried out using robust linear regression models both in the exploratory EWAS analyses and in the look-up of the PACE findings in infant saliva. Results None of the cord blood birthweight-associated CpGs identified by the PACE Consortium was associated with birthweight when analysed in infant saliva. In saliva EWAS analyses, considering a false discovery rate p-values < 0.05, birthweight as continuous variable was associated with DNA methylation in 44 CpG sites; being born small for gestational age (SGA, lower 10th percentile of birthweight for gestational age according to WHO reference charts) was associated with DNA methylation in 44 CpGs, with only one overlapping CpG between the two analyses. Despite no overlap with PACE results at the CpG level, two of the top saliva birthweight CpGs mapped at genes associated with birthweight with the same direction of the effect also in the PACE Consortium (MACROD1 and RPTOR). Conclusion Our study provides an indication of the birthweight and SGA epigenetic salivary signatures in children around 10 months of age. DNA methylation signatures in cord blood may not be comparable with saliva DNA methylation signatures at about 10 months of age, suggesting that the birthweight epigenetic marks are likely time and tissue specific.

scholarly journals Associations of circulating folate, vitamin B12 and homocysteine concentrations in early pregnancy and cord blood with epigenetic gestational age: the Generation R Study

2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Giulietta S. Monasso ◽  
Leanne K. Küpers ◽  
Vincent W. V. Jaddoe ◽  
Sandra G. Heil ◽  
Janine F. Felix
Keyword(s):  
Dna Methylation ◽  
Vitamin B12 ◽  
Cord Blood ◽  
Gestational Age ◽  
Fetal Development ◽  
Maternal Plasma ◽  
Plasma Homocysteine ◽  
Training Population ◽  
Epigenetic Aging ◽  
Pregnancy Dating

Abstract Background Circulating folate, vitamin B12 and homocysteine concentrations during fetal development have been associated with health outcomes in childhood. Changes in fetal DNA methylation may be an underlying mechanism. This may be reflected in altered epigenetic aging of the fetus, as compared to chronological aging. The difference between gestational age derived in clinical practice and gestational age predicted from neonatal DNA methylation data is referred to as gestational age acceleration. Differences in circulating folate, vitamin B12 and homocysteine concentrations during fetal development may be associated with gestational age acceleration. Results Up to 1346 newborns participating in the Generation R Study, a population-based prospective cohort study, had both cord blood DNA methylation data available and information on plasma folate, serum total and active B12 and plasma homocysteine concentrations, measured in early pregnancy and/or in cord blood. A subgroup of 380 newborns had mothers with optimal pregnancy dating based on a regular menstrual cycle and a known date of last menstrual period. For comparison, gestational age acceleration was calculated based the method of both Bohlin and Knight. In the total study population, which was more similar to Bohlin’s training population, one standard deviation score (SDS) higher maternal plasma homocysteine concentrations was nominally associated with positive gestational age acceleration [0.07 weeks, 95% confidence interval (CI) 0.02, 0.13] by Bohlin’s method. In the subgroup with pregnancy dating based on last menstrual period, the method that was also used in Knight’s training population, one SDS higher cord serum total and active B12 concentrations were nominally associated with negative gestational age acceleration [(− 0.16 weeks, 95% CI − 0.30, − 0.02) and (− 0.15 weeks, 95% CI − 0.29, − 0.01), respectively] by Knight’s method. Conclusions We found some evidence to support associations of higher maternal plasma homocysteine concentrations with positive gestational age acceleration, suggesting faster epigenetic than clinical gestational aging. Cord serum vitamin B12 concentrations may be associated with negative gestational age acceleration, indicating slower epigenetic than clinical gestational aging. Future studies could examine whether altered fetal epigenetic aging underlies the associations of circulating homocysteine and vitamin B12 blood concentrations during fetal development with long-term health outcomes.

scholarly journals DNA methylation in cord blood as mediator of the association between prenatal arsenic exposure and gestational age

Epigenetics ◽  
2018 ◽  
Vol 13 (9) ◽  
pp. 923-940 ◽  
Author(s):  
Anne K. Bozack ◽  
Andres Cardenas ◽  
Quazi Quamruzzaman ◽  
Mahmuder Rahman ◽  
Golam Mostofa ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Cord Blood ◽  
Gestational Age ◽  
Arsenic Exposure

scholarly journals Replicated umbilical cord blood DNA methylation loci associated with gestational age at birth

Epigenetics ◽  
2020 ◽  
Vol 15 (11) ◽  
pp. 1243-1258 ◽  
Author(s):  
Timothy P. York ◽  
Shawn J. Latendresse ◽  
Colleen Jackson-Cook ◽  
Dana M. Lapato ◽  
Sara Moyer ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Cord Blood ◽  
Umbilical Cord ◽  
Umbilical Cord Blood ◽  
Gestational Age ◽  
Gestational Age At Birth ◽  
Age At Birth

scholarly journals Differential DNA methylation profile in infants born small-for-gestational-age: association with markers of adiposity and insulin resistance from birth to age 24 months

2020 ◽  
Vol 8 (1) ◽  
pp. e001402
Author(s):  
Marta Diaz ◽  
Edurne Garde ◽  
Abel Lopez-Bermejo ◽  
Francis de Zegher ◽  
Lourdes Ibañez
Keyword(s):  
Insulin Resistance ◽  
Dna Methylation ◽  
Body Composition ◽  
Cord Blood ◽  
Gestational Age ◽  
Small For Gestational Age ◽  
Diabetes Risk ◽  
Metabolic Dysfunction ◽  
A Genome ◽  
Methylation Profiling

IntroductionPrenatal growth restraint followed by rapid postnatal weight gain increases lifelong diabetes risk. Epigenetic dysregulation in critical windows could exert long-term effects on metabolism and confer such risk.Research design and methodsWe conducted a genome-wide DNA methylation profiling in peripheral blood from infants born appropriate-for-gestational-age (AGA, n=30) or small-for-gestational-age (SGA, n=21, with postnatal catch-up) at age 12 months, to identify new genes that may predispose to metabolic dysfunction. Candidate genes were validated by bisulfite pyrosequencing in the entire cohort. All infants were followed since birth; cord blood methylation profiling was previously reported. Endocrine-metabolic variables and body composition (dual-energy X-ray absorptiometry) were assessed at birth and at 12 and 24 months.ResultsGPR120 (cg14582356, cg01272400, cg23654127, cg03629447), NKX6.1 (cg22598426, cg07688460, cg17444738, cg12076463, cg10457539), CPT1A (cg14073497, cg00941258, cg12778395) and IGFBP 4 (cg15471812) genes were hypermethylated (GPR120, NKX6.1 were also hypermethylated in cord blood), whereas CHGA (cg13332653, cg15480367, cg05700406), FABP5 (cg00696973, cg10563714, cg16128701), CTRP1 (cg19231170, cg19472078, cg0164309, cg07162665, cg17758081, cg18996910, cg06709009), GAS6 (N/A), ONECUT1 (cg14217069, cg02061705, cg26158897, cg06657050, cg15446043) and SLC2A8 (cg20758474, cg19021975, cg11312566, cg12281690, cg04016166, cg03804985) genes were hypomethylated in SGA infants. These genes were related to β-cell development and function, inflammation, and glucose and lipid metabolism and associated with body mass index, body composition, and markers of insulin resistance at 12 and 24 months.ConclusionIn conclusion, at 12 months, abnormal methylation of GPR120 and NKX6.1 persists and new epigenetic marks further involved in adipogenesis and energy homeostasis arise in SGA infants. These abnormalities may contribute to metabolic dysfunction and diabetes risk later in life.

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