Epigenetics and the placenta

Nelissen, E. C. M.; Montfoort, Aafke P.A. van; Dumoulin, J.C.M.; Evers, Johannes L.H.

doi:10.1093/humupd/dmq052

Cited by 330 publications

(248 citation statements)

References 201 publications

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“…These differences appear to persist throughout embryonic development (Nelissen et al, 2011;RuggGunn, 2012). Global DNA methylation is lower in the trophectoderm than in the inner cell mass of the blastocyst, and this lower methylation is retained in the extra-embryonic tissue compared with the somatic tissue (Santos et al, 2002).…”

Section: Epigenetics Placental Function and Nutritionmentioning

confidence: 99%

Placental contribution to nutritional programming of health and diseases: epigenetics and sexual dimorphism

Tarrade

Panchenko

Junien

et al. 2015

Journal of Experimental Biology

207

149

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The recent and rapid worldwide increase in non-communicable diseases challenges the assumption that genetic factors are the primary contributors to such diseases. A new concept of the 'developmental origins of health and disease' (DOHaD) is at stake and therefore requires a paradigm shift. Maternal obesity and malnutrition predispose offspring to develop metabolic syndrome, a vicious cycle leading to transmission to subsequent generation(s), with differences in response and susceptibility according to the sex of the individual. The placenta is a programming agent of adult health and disease. Adaptations of placental phenotype in response to maternal diet and metabolic status alter fetal nutrient supply. This implies important epigenetic changes that are, however, still poorly documented in DOHaD studies, particularly concerning overnutrition. The aim of this review is to discuss the emerging knowledge on the relationships between the effect of maternal nutrition or metabolic status on placental function and the risk of diseases later in life, with a specific focus on epigenetic mechanisms and sexual dimorphism. Explaining the sex-specific causal variables and how males versus females respond and adapt to environmental perturbations should help physicians and patients to anticipate disease susceptibility.KEY WORDS: DOHaD, Fetal programming, Placenta, Sex, Nutrition, Obesity, Maternal environment, Gestation Introduction: developmental origins of health and diseaseThe recent and rapid worldwide increase in non-communicable diseases (NCDs) challenges the assumption that genetic factors are the primary contributors to such diseases (McAllister et al., 2009). The 'developmental origins of health and disease' (DOHaD) paradigm states that the environment during the periconception, gestation and lactation periods shapes the developing individuals, leading, in the case of a deleterious environment, to a predisposition to adult-onset diseases. This theory was popularised by D. J. Barker in the early 1990s (Barker, 1990) but the question had already been raised in earlier studies. In the 1960s and 1970s, different experiments on diverse mammalian species (rat, mouse, guinea pig, pig, etc.) showed that a reduction of maternal calorie or protein intake during pregnancy and lactation affects the growth capacity and cognitive ability of the offspring (reviewed in Roeder and Chow, 1972;McCance, 1976). Later, this concept was extended to phenotype in general, with a strong implication for quantitative traits in agriculture. An increasing number of studies pointed to the fact that maternal environment in cattle was an important parameter to fully express the genetically highly selected potential of the animals (Wallace et al., 2010; Jammes et al., 2011;Tanghe et al., 2014).Male and female susceptibility to NCDs is well described. It appears that in the DOHaD context, the same environmental exposure may affect the long-term health of the offspring with a discrepancy between males and females in terms of the timing, onset ...

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Section: Epigenetics Placental Function and Nutritionmentioning

confidence: 99%

Placental contribution to nutritional programming of health and diseases: epigenetics and sexual dimorphism

Tarrade

Panchenko

Junien

et al. 2015

Journal of Experimental Biology

207

149

View full text Add to dashboard Cite

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“…The enzyme used to catalyze DNA methylation is DNA methyltransference (DNMTs) that included DNMT1, DNMT3a, DNMT3b and DNMT3l, in which DNMT1, as the persistent one, mainly participate in the maintenance of methylation condition, whereas DNMT3a and DNMT3b, as the de nove methyltransferences, can methylate CpG (Nelissen et al, 2011). DNA methylation has been widely used for the early diagnosis of malignant tumors such as leukemia, non-small cell lung cancer and renal cell carcinoma (Nordlund et al, 2015;Guo et al, 2015;Karami et al, 2015).…”

Section: Discussionmentioning

confidence: 99%

Application of Multiplex Nested Methylated Specific PCR in Early Diagnosis of Epithelial Ovarian Cancer

Bi¹,

Yu²,

Yang³

et al. 2015

Asian Pacific Journal of Cancer Prevention

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Objective: To explore the application of multiplex nested methylated specific polymerase chain reaction (PCR) in the early diagnosis of epithelial ovarian carcinoma (EOC). Materials and Methods: Serum and fresh tissue samples were collected from 114 EOC patients. RUNX3, TFPI2 and OPCML served as target genes. Methylation levels of tissues were assessed by multiplex nested methylated specific PCR, the results being compared with those for carcinoma antigen 125 (CA125). Results: The serum free deoxyribose nucleic acid (DNA) methylation spectrum of EOC patients was completely contained in the DNA spectrum of cancer tissues, providing an accurate reflection of tumor DNA methylation conditions. Serum levels of CA125 and free DNA methylation in the EOC group were evidently higher than those in benign lesion and control groups (p<0.05). Patients with early EOC had markedly lower serum CA125 than those with advanced EOC (p<0.05), but there was no significant difference in free DNA methylation (p>0.05). The sensitivity, specificity and positive predicative value (PPV) of multiplex nested methylated specific PCR were significantly higher for detection of all patients and those with early EOC than those for CA125 (p<0.05). In the detection of patients with advanced EOC, the PPV of CA125 detection was obviously lower than that of multiplex nested methylated specific PCR (p>0.05), but there was no significant difference in sensitivity (p>0.05). Conclusions: Serum free DNA methylation can be used as a biological marker for EOC and multiplex nested methylated specific PCR should be considered for early diagnosis since it can accurately determine tumor methylation conditions.

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“…Because the intrauterine environment of MZ twins can differ, it is possible that intrauterine differences contribute to differences in epigenetic states. Studies investigating placental epigenetic dysregulation have identified altered DNA methylation of genes involved in placental development, including trophoblast differentiation, angiogenesis, and endocrine signaling (28). Placental epigenetic dysregulation, in particular altered DNA methylation, has been proposed as a mechanism underlying the aberrant gene expression in the pathophysiology of IUGR.…”

Section: The Discordant Mz Twin Model and Epigeneticsmentioning

confidence: 99%

Epigenetic Basis of Twin Discordance in Diseases: Future Benefits

Demir

2018

Gynecol Obstet Reprod Med

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Monozygotic twins share the same genotype since they are derived from the same zygote. However, monozygotic twin siblings frequently present many phenotypic differences, such as their susceptibilities to diseases. These isogenic individuals are not entirely identical. They exhibit phenotypic incompatibility for many features, from birth weight to complex diseases. Recently, several studies have been published showing that phenotypic differences, especially in monozygotic twins, are being induced from prenatal period to life-long epigenetic differences. Epigenetic studies on twins have a great potential to contribute to our understanding of complex diseases, such as cancer, autoimmune disorders, psychiatric disorders and neurological diseases. Since monozygotic twins are genetic clones (genetically identical), they are considered as perfect models for studying the role of environmental factors as determinants of complex diseases and phenotypes. In this review, a number of intrauterine effects and genetic mechanisms that may affect phenotypic, genotypic, and epigenetic differences between monozygotic twins were described and effects of epigenetic mechanisms on complex diseases were mentioned. Further work on epigenetic changes in diseases using incompatible monozygotic twin models, would lead to new developments in medical therapies.

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Epigenetics and the placenta

Cited by 330 publications

References 201 publications

Placental contribution to nutritional programming of health and diseases: epigenetics and sexual dimorphism

Placental contribution to nutritional programming of health and diseases: epigenetics and sexual dimorphism

Application of Multiplex Nested Methylated Specific PCR in Early Diagnosis of Epithelial Ovarian Cancer

Epigenetic Basis of Twin Discordance in Diseases: Future Benefits

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