Maternal smoking during pregnancy and cord blood DNA methylation: new insight on sex differences and effect modification by maternal folate levels

Zhang, Boyang; Hong, Xiumei; Ji, Hongkai; Tang, Wan Yee; Kimmel, Mary; Ji, Yuelong; Pearson, Colleen; Zuckerman, Barry; Surkan, Pamela J.; Wang, Xiaobin

doi:10.1080/15592294.2018.1475978

Cited by 36 publications

(31 citation statements)

References 53 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Interestingly, the impact of prenatal cigarette smoke on DNA methylation may be gender-specific. It was shown that the male fetus is more susceptible to maternal smoking than the female [110], and the alteration of DNA methylation in the differentially methylated region (DMR) of the IGF2 gene was more notable among newborn boys than girls [105], whereas Bouwland-Both reported an adverse result [111]. Moreover, a study has shown that maternal smoking showed a much stronger impact on offspring methylation intensity than paternal smoking [15] (Table 1).…”

Section: Prenatal Environmental Pollution and Epigenetic Dysregulationmentioning

confidence: 99%

“…Dynamic processes of epigenetic reprogramming in male and female genomes exhibit dramatic differences [14, 20] and this includes changes to the epigenome in their embryonic stem cells [249]. As aforementioned, male fetus has been observed a higher susceptibility to maternal smoking than the female [110]. Developmental exposure to vinclozolin [156] and BPA [146–148] has been shown a transgenerational inheritance of aberrant methylation patterns through the male germ line.…”

Section: Prenatal Environmental Pollution and Epigenetic Dysregulationmentioning

confidence: 99%

See 1 more Smart Citation

Prenatal epigenetics diets play protective roles against environmental pollution

2019

View full text Add to dashboard Cite

It is thought that germ cells and preimplantation embryos during development are most susceptible to endogenous and exogenous environmental factors because the epigenome in those cells is undergoing dramatic elimination and reconstruction. Exposure to environmental factors such as nutrition, climate, stress, pathogens, toxins, and even social behavior during gametogenesis and early embryogenesis has been shown to influence disease susceptibility in the offspring. Early-life epigenetic modifications, which determine the expression of genetic information stored in the genome, are viewed as one of the general mechanisms linking prenatal exposure and phenotypic changes later in life. From atmospheric pollution, endocrine-disrupting chemicals to heavy metals, research increasingly suggests that environmental pollutions have already produced significant consequences on human health. Moreover, mounting evidence now links such pollution to relevant modification in the epigenome. The epigenetics diet, referring to a class of bioactive dietary compounds such as isothiocyanates in broccoli, genistein in soybean, resveratrol in grape, epigallocatechin-3-gallate in green tea, and ascorbic acid in fruits, has been shown to modify the epigenome leading to beneficial health outcomes. This review will primarily focus on the causes and consequences of prenatal environment pollution exposure on the epigenome, and the potential protective role of the epigenetics diet, which could play a central role in neutralizing epigenomic aberrations against environmental pollutions.

show abstract

Section: Prenatal Environmental Pollution and Epigenetic Dysregulationmentioning

confidence: 99%

Section: Prenatal Environmental Pollution and Epigenetic Dysregulationmentioning

confidence: 99%

Prenatal epigenetics diets play protective roles against environmental pollution

2019

View full text Add to dashboard Cite

show abstract

“…[15]. Despite the common use of CB as an epigenetic surrogate of neonates, several published studies involve the correction of epigenetic data based on cell type population of CB specimens using microarray [48–50], and the requirement of such correction in the future studies may introduce significant complexity into CB-based epigenetic studies using other methods. Recently, Lin et al .…”

Section: Discussionmentioning

confidence: 99%

DNA methylome of human neonatal umbilical cord: Enrichment of differentially methylated regions compared to umbilical cord blood DNA at transcription factor genes involved in body patterning and effects of maternal folate deficiency or children’s sex

et al. 2019

View full text Add to dashboard Cite

The DOHaD (developmental origins of health and disease) hypothesis claims that fetal malnutrition or exposure to environmental pollutants may affect their lifelong health. Epigenetic changes may play significant roles in DOHaD; however, access to human fetuses for research has ethical and technical hurdles. Umbilical cord blood (CB) has been commonly used as an epigenetic surrogate of fetuses, but it does not provide direct evidence of fetal exposure to pollutants. Here, we propose umbilical cord tissue (UC), which accumulates substances delivered to fetuses during gestation, as an alternative surrogate for epigenetic studies on fetuses. To explore the feasibility to examine UC epigenome by deep sequencing, we determined CpG methylation profiles of human postnatal UC by reduced representation bisulfite sequencing. Principal component analysis clearly separated the DNA methylomes of UC and CB pairs isolated from the same newborn (n = 10). Although all UC chromosomes were modestly hypomethylated compared to CB chromosomes, GO analysis revealed strong enrichment of differentially methylated regions (DMRs) at promoter-associated CpG islands in the HOX gene clusters and other genes encoding transcription factors involved in determination of the body pattern. DNA methylomes of UC autosomes were largely comparable between males and females. Deficiency of folate during pregnancy has been suggested to affect fetal DNA methylation to cause congenital anomalies. Whereas DNA methylome of UC was not significantly affected by early-gestational (12 weeks) low levels of maternal plasma folate (< 8 ng/ml, n = 10) compared to controls (>19 ng/mL, n = 10), two specific loci of LTR12C endogenous retroviruses in chromosome 12 were significantly hypermethylated in the low-folate group. Our study suggests that UC is useful as an alternative surrogate for studying environmental effects on DNA methylation in human fetuses, compensating CB by providing additional information about epigenetic regulation of genes involved in developmental body patterning and endogenous retroviruses.

show abstract

“…Demethylation of AHRR in the cord blood of children with prenatal smoking exposure is broadly reported. One recent study further discovered the interactive effect of maternal smoking and high folate level, suggesting that adequate maternal folate levels attenuate the impact of smoking on the hypomethylation of AHRR [118]. As these studies mature and elaborate on these co-exposure effects, we may be able to better classify and understand the epigenetic plasticity to the complexity and mixture of exposures.…”

Section: Challenges and Outlookmentioning

confidence: 99%

Environmentally Induced Epigenetic Plasticity in Development: Epigenetic Toxicity and Epigenetic Adaptation

Tian

Marsit

2018

Curr Epidemiol Rep

View full text Add to dashboard Cite

Purpose of Review Epigenetic processes represent important mechanisms underlying developmental plasticity in response to environmental exposures. The current review discusses three classes of environmentally-induced epigenetic changes reflecting two aspects of that plasticity, toxicity effects as well as adaptation in the process of development. Recent findings Due to innate resilience, epigenetic changes caused by environmental exposures may not always lead impairments but may allow the organisms to achieve positive developmental outcomes through appropriate adaptation and a buffering response. Thus, some epigenetic adaptive responses to an immediate stimulus or exposure early in life would be expected to have a survival advantage but these same responses may also result in adverse developmental outcomes as they persists into later life stage. Although accumulating literature has identified environmentally induced epigenetic changes and linked them to health outcomes, we currently face challenges in the interpretation of the functional impact of their epigenetic plasticity. Summary Current environmental epigenetic research suggest that epigenetic processes may serve as a mechanism for resilience, and that they can be considered in terms of their impact on toxicity as a negative outcome, but also on adaptation for improved survival or health. This review encourages epigenetic environmental studies to move deeper inside into the functional meaning of epigenetic plasticity in the development.

show abstract

Maternal smoking during pregnancy and cord blood DNA methylation: new insight on sex differences and effect modification by maternal folate levels

Cited by 36 publications

References 53 publications

Prenatal epigenetics diets play protective roles against environmental pollution

Prenatal epigenetics diets play protective roles against environmental pollution

DNA methylome of human neonatal umbilical cord: Enrichment of differentially methylated regions compared to umbilical cord blood DNA at transcription factor genes involved in body patterning and effects of maternal folate deficiency or children’s sex

Environmentally Induced Epigenetic Plasticity in Development: Epigenetic Toxicity and Epigenetic Adaptation

Contact Info

Product

Resources

About