Genome-Wide Analysis of DNA Methylation in Human Amnion

Kim, Jinsil; Pitlick, Mitchell M.; Christine, Paul J.; Schaefer, Amanda R.; Saleme, César; Comas, Belén; Cosentino, Viviana; Gadow, Enrique C.; Murray, Jeffrey C.

doi:10.1201/b16304-4

Cited by 16 publications

(22 citation statements)

References 51 publications

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“…Studies have suggested that maternal factors, including socioeconomic status [11], pre-pregnancy BMI [26], smoking during pregnancy [27] and nutrition status [28] affect the risk of PTB. DNA methylation partially explains the effects many of these factors [19][20][21][22][23][24][26][27][28]. In this study, we found associations of maternal BMI, delivery season and WBC count with PTB; however, these factors did not in uence the DNA methylation levels of VTRNA2-1 in maternal blood.…”

Section: Discussioncontrasting

confidence: 52%

“…DNA methylation changes in the amnion or foetal tissue were determined to be partially involved in the physiological process of PTB and in foetal development. [23,24]. Thus, the evaluation of genes containing these differentially methylated sites may be useful to identify biological pathways involved in PTB, thereby facilitating the identi cation of clinically informative biomarkers for the prediction of PTB.…”

Section: Introductionmentioning

confidence: 99%

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Hypermethylation of the VTRNA2-1 promoter in maternal blood is associated with preterm birth

You¹,

Kwon²,

Hwang³

et al. 2020

Preprint

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Background: Preterm birth is associated with an increased risk of neonatal complications and death, as well as poor health and disease later in life. Epigenetics could contribute to the mechanism underlying preterm birth. Results: Genome-wide DNA methylation analysis of whole blood cells from ten women was performed using an Illumina Infinium HumanMethylation450 BeadChips array. We identified 1,581 differentially methylated CpG sites in promotor regions between term and preterm birth. Although the differences were not significant after correcting for multiple tests, seven CpGs on the genomically imprinted VTRNA2-1 showed the largest differences (range: 26–39%). Pyrosequencing verification was performed with blood samples from pregnant women recruited additionally (n = 82). In total, 28 (34.1%) cases showed hypomethylation of the VTRNA2-1 promoter (< 13% methylation), while 54 cases (65.9%) showed a methylation level of 30–60%. Hypermethylation of VTRNA2-1 was associated with an increased risk of preterm birth after adjusting for maternal age, season of delivery, parity and white blood cell count. The mRNA expression of VTRNA2-1 was 0.51-fold lower in women with preterm deliveries (n = 20) compared with women with term deliveries (n = 20). Conclusions: Our results suggest that changes in VTRNA2-1 methylation in maternal blood are related to preterm birth. Further studies are needed to confirm the association of VTRNA2-1 methylation with preterm birth in a large population, and to elucidate the underlying mechanism.

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Section: Discussioncontrasting

confidence: 52%

Section: Introductionmentioning

confidence: 99%

Hypermethylation of the VTRNA2-1 promoter in maternal blood is associated with preterm birth

You¹,

Kwon²,

Hwang³

et al. 2020

Preprint

View full text Add to dashboard Cite

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“…38,44 DNA methylation patterns regulate the functional properties of immune cells 45,46 and associate with inflammatory markers, 47 chronic disorders, [48][49][50] and PTB. 27,51 We hypothesize that DNA methylation patterns may reveal genes whose regulation is unique to women who deliver preterm or provide insight into its intergenerational risk…”

Section: Introductionmentioning

confidence: 99%

DNA methylation provides insight into intergenerational risk for preterm birth in African Americans

et al. 2015

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Abbreviations: DOHaD, developmental origin of health and disease; FDR, false discovery rate; GA, gestational age; PTB, preterm birth; SES, socioeconomic status.African Americans are at increased risk for spontaneous preterm birth (PTB). Though PTB is heritable, genetic studies have not identified variants that account for its intergenerational risk, prompting the hypothesis that epigenetic factors may also contribute. The objective of this study was to evaluate DNA methylation from maternal leukocytes to identify patterns specific to PTB and its intergenerational risk. DNA from peripheral leukocytes from African American women that delivered preterm (24-34 weeks; N D 16) or at term (39-41 weeks; N D 24) was assessed for DNA methylation using the HumanMethylation450 BeadChip. In maternal samples, 17,829 CpG sites associated with PTB, but no CpG site remained associated after correction for multiple comparisons. Examination of paired maternal-fetal samples identified 5,171 CpG sites in which methylation of maternal samples correlated with methylation of her respective fetus (FDR < 0.05). These correlated sites were enriched for association with PTB in maternal leukocytes. The majority of correlated CpG sites could be attributed to one or more genetic variants. They were also significantly more likely to be in genes involved in metabolic, cardiovascular, and immune pathways, suggesting a role for genetic and environmental contributions to PTB risk and chronic disease. The results of this study may provide insight into the factors underlying intergenerational risk for PTB and its consequences.

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“…Methylation of the third intron of the human OXTR was associated with repressive binding proteins from non-expressing peripheral blood leukocytes, while relative hypomethylation of this region was associated with myometrium from non-pregnant and term pregnancy (Mizumoto et al, 1997). Kim et al (2013) assessed some methyl sites in the 5' UTR of the OXTR in term, pre-term labored and term unlabored amnion. Methylation of the human OXTR gene predominantly at a site called MT2 contributes to tissue-specific repression of OXTR mRNA expression, in vitro (Kusui et al, 2001) and is associated with OXTR mRNA repression in human brain (Gregory et al, 2009).…”

Section: Gene By Environment Interactionsmentioning

confidence: 99%

Developmental Perspectives on Oxytocin and Vasopressin

Hammock

2014

Neuropsychopharmacol

153

146

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The related neuropeptides oxytocin and vasopressin are involved in species-typical behavior, including social recognition behavior, maternal behavior, social bonding, communication, and aggression. A wealth of evidence from animal models demonstrates significant modulation of adult social behavior by both of these neuropeptides and their receptors. Over the last decade, there has been a flood of studies in humans also implicating a role for these neuropeptides in human social behavior. Despite popular assumptions that oxytocin is a molecule of social bonding in the infant brain, less mechanistic research emphasis has been placed on the potential role of these neuropeptides in the developmental emergence of the neural substrates of behavior. This review summarizes what is known and assumed about the developmental influence of these neuropeptides and outlines the important unanswered questions and testable hypotheses. There is tremendous translational need to understand the functions of these neuropeptides in mammalian experience-dependent development of the social brain. The activity of oxytocin and vasopressin during development should inform our understanding of individual, sex, and species differences in social behavior later in life.

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Genome-Wide Analysis of DNA Methylation in Human Amnion

Cited by 16 publications

References 51 publications

Hypermethylation of the VTRNA2-1 promoter in maternal blood is associated with preterm birth

Hypermethylation of the VTRNA2-1 promoter in maternal blood is associated with preterm birth

DNA methylation provides insight into intergenerational risk for preterm birth in African Americans

Developmental Perspectives on Oxytocin and Vasopressin

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