Adaptations of placental and cord blood<i>ABCA1 </i>DNA methylation profile to maternal metabolic status

Houde, Andrée-Anne; Guay, Simon-Pierre; Desgagné, Véronique; Hivert, Marie‐France; Baillargeon, Jean-Patrice; St‐Pierre, Julie; Perron, Patrice; Gaudet, Daniel; Brisson, Diane; Bouchard, Luigi

doi:10.4161/epi.26554

Cited by 88 publications

(71 citation statements)

References 57 publications

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“…Interestingly, the correlation trend between PPARGC1A methylation in cord blood and gestational glycaemia was antithetical to that of placenta, similar to the findings of others [19], supporting the notion that DNA methylation patterns of specific genes can vary among tissues. The disparate epigenetic signature of an organ or tissue may reflect their different functions [43][44][45][46].…”

Section: Discussionsupporting

confidence: 82%

“…A previous study revealed that chronic exposure to a hyperglycaemic environment can lead to persistent alterations in DNA methylation of metabolic genes in Schwann cells [53]. Placental DNA methylation is responsive to intrauterine hyperglycaemia, as demonstrated in the present study by the correlations between maternal gestational glycaemia and the DNA methylation of PPARGC1A as well as other genes involved in energy homoeostasis [16,18,19,54]. The alterations in placental DNA methylation can disturb placental function which may contribute to disease susceptibility in later life [22].…”

Section: Discussionmentioning

confidence: 52%

“…Being highly responsive to various environmental factors including nutrient signals, epigenetic modifications could conceivably predispose to placental dysfunction [22]. And, in concordance with this premise, placental DNA methylation of LEP [16,17], ADIPOQ [18] and ABCA1 [19] genes are associated with maternal gestational glycaemia, inferring that impaired placental function is mediated by epigenetic modifications [22].…”

Section: Introductionmentioning

confidence: 94%

“…Most An adverse intrauterine environment, complicated by either undernutrition [14] or overfeeding [15], may programme harmful metabolic consequences later in life through epigenetic modifications such as DNA methylation. For instance, maternal gestational glycaemia concentrations correlate with placental DNA methylation adaptations of LEP (leptin) [16,17], ADIPOQ (adiponectin, C1Q and collagen domain-containing) [18] and ABCA1 (ATPbinding cassette transporter A1) [19] genes. Although the tenet of fetal metabolic programming has been extensively explored in animal models [20,21], only a small number of studies on epigenetic modification have been conducted in humans, especially in those with GDM.…”

Section: Introductionmentioning

confidence: 99%

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Placental DNA methylation of peroxisome-proliferator-activated receptor-γ co-activator-1α promoter is associated with maternal gestational glucose level

et al. 2015

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Intrauterine exposure to hyperglycaemia may increase the risk of later-life metabolic disorders. Although the underlying mechanism is not fully understood, epigenetic dysregulation in fetal programming has been implicated. With regard to energy homoeostasis, PGC-1α (peroxisome-proliferator-activated receptor γ co-activator-1α, encoded by the PPARGC1A gene) plays a regulatory role in several biochemical processes. We hypothesized that maternal gestational glucose levels would positively correlate with DNA methylation of the PPARGC1A promoter in placental tissue. We undertook a cross-sectional study of 58 mothers who underwent uncomplicated Caesarean delivery in a university hospital. Maternal gestational glucose concentration was determined after a 75-g OGTT (oral glucose tolerance test) at 24-28 weeks of gestation. Placenta tissue and cord blood were collected immediately after delivery. Genomic DNA was extracted and thereafter bisulfite conversion was performed. After PCR amplification, the DNA methylation of the PPARGC1A promoter was quantified using a pyrosequencing technique. The protein level of PGC-1α was evaluated by Western blotting. For all participants as a whole, including the GDM (gestational diabetes mellitus) and normoglycaemia groups, the maternal gestational glucose level was positively correlated with placental DNA methylation, and negatively correlated with cord blood DNA methylation of the PPARGC1A promoter in a CpG site-specific manner. In the GDM group alone, the placental CpG site-specific methylation of the PPARGC1A promoter strongly correlated with gestational 2-h post-OGTT glycaemia. Epigenetic alteration of the PPAGRC1A promoter may be one of the potential mechanisms underlying the metabolic programming in offspring exposed to intrauterine hyperglycaemia.

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Section: Discussionsupporting

confidence: 82%

Section: Discussionmentioning

confidence: 52%

Section: Introductionmentioning

confidence: 94%

Section: Introductionmentioning

confidence: 99%

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Placental DNA methylation of peroxisome-proliferator-activated receptor-γ co-activator-1α promoter is associated with maternal gestational glucose level

et al. 2015

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“…The different blood MEST methylation was also observed in morbid obese adults compared with normal-weight controls. Further studies showed that the DNA methylation levels of ATP-binding cassette transporter A1 in cord blood and placental tissues were associated with glucose and cord blood triglyceride levels [32]. These independent studies all indicate that epigenetic changes could contribute to explaining the detrimental health effects associated with fetal programming, such as increased risk of obesity and type 2 diabetes mellitus in offspring of diabetic mothers.…”

Section: Epigenetics and Candidate Genesmentioning

confidence: 95%

Maternal Diabetes Mellitus and the Origin of Non-Communicable Diseases in Offspring: The Role of Epigenetics1

Zhang

Schatten

et al. 2014

Biology of Reproduction

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Offspring of diabetic mothers are susceptible to the onset of metabolic syndromes, such as type 2 diabetes and obesity at adulthood, and this trend can be inherited between generations. Genetics cannot fully explain how the noncommunicable disease in offspring of diabetic mothers is caused and inherited by the next generations. Many studies have confirmed that epigenetics may be crucial for the detrimental effects on offspring exposed to the hyperglycemic environment. Although the adverse effects on epigenetics in offspring of diabetic mothers may be the result of the poor intrauterine environment, epigenetic modifications in oocytes of diabetic mothers are also affected. Therefore, the present review is focused on the epigenetic alterations in oocytes and embryos of diabetic mothers. Furthermore, we also discuss initial mechanistic insight on maternal diabetes mellitus causing alterations of epigenetic modifications.

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Maternal weight affects placental DNA methylation of genes involved in metabolic pathways in the common marmoset monkey (Callithrix jacchus)

Narapareddy

Wildman

Armstrong

et al. 2020

American J Primatol

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Accumulating evidence suggests that dysregulation of placental DNA methylation (DNAm) is a mechanism linking maternal weight during pregnancy to metabolic programming outcomes. The common marmoset, Callithrix jaccus, is a platyrrhine primate species that has provided much insight into studies of the primate placenta, maternal condition, and metabolic programming, yet the relationships between maternal weight and placental DNAm are unknown. Here, we report genome‐wide DNAm from term marmoset placentas using reduced representation bisulfite sequencing. We identified 74 genes whose DNAm pattern is associated with maternal weight during gestation. These genes are predominantly involved in energy metabolism and homeostasis, including the regulation of glycolytic and lipid metabolic processes pathways.

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Adaptations of placental and cord bloodABCA1 DNA methylation profile to maternal metabolic status

Cited by 88 publications

References 57 publications

Placental DNA methylation of peroxisome-proliferator-activated receptor-γ co-activator-1α promoter is associated with maternal gestational glucose level

Placental DNA methylation of peroxisome-proliferator-activated receptor-γ co-activator-1α promoter is associated with maternal gestational glucose level

Maternal Diabetes Mellitus and the Origin of Non-Communicable Diseases in Offspring: The Role of Epigenetics1

Maternal weight affects placental DNA methylation of genes involved in metabolic pathways in the common marmoset monkey (Callithrix jacchus)

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