Effect of folate deficiency on placental DNA methylation in hyperhomocysteinemic rats

Kim, Ji-Myung; Hong, Kyungju; Lee, Ji Hye; Lee, Suman; Chang, Namsoo

doi:10.1016/j.jnutbio.2008.01.010

Cited by 84 publications

(59 citation statements)

References 29 publications

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“…For example, maternally derived micronutrients such as folate and choline serve as substrates for DNA methyltransferases (DNMT) and their deficiency decreases placental DNA methylation (Kim et al, 2009). In calorie-restricted as well as high-fat diet-exposed mice, distinct hypomethylation patterns were detected in male and female placentas, including at imprinted loci, suggesting sex-specific placental adaptive responses to nutritional state GallouKabani et al, 2010).…”

Section: Encoding Of Stress Memories In the Epigenomementioning

confidence: 99%

The Placenta as a Mediator of Stress Effects on Neurodevelopmental Reprogramming

Bronson

Bale

2015

Neuropsychopharmacol

205

180

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Adversity experienced during gestation is a predictor of lifetime neuropsychiatric disease susceptibility. Specifically, maternal stress during pregnancy predisposes offspring to sex-biased neurodevelopmental disorders, including schizophrenia, attention deficit/hyperactivity disorder, and autism spectrum disorders. Animal models have demonstrated disease-relevant endophenotypes in prenatally stressed offspring and have provided unique insight into potential programmatic mechanisms. The placenta has a critical role in the deleterious and sex-specific effects of maternal stress and other fetal exposures on the developing brain. Stress-induced perturbations of the maternal milieu are conveyed to the embryo via the placenta, the maternal-fetal intermediary responsible for maintaining intrauterine homeostasis. Disruption of vital placental functions can have a significant impact on fetal development, including the brain, outcomes that are largely sex-specific. Here we review the novel involvement of the placenta in the transmission of the maternal adverse environment and effects on the developing brain.

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Section: Encoding Of Stress Memories In the Epigenomementioning

confidence: 99%

The Placenta as a Mediator of Stress Effects on Neurodevelopmental Reprogramming

Bronson

Bale

2015

Neuropsychopharmacol

205

180

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“…In fact, Fuso and co-workers demonstrated that β-secretase (Bace) and presenilin 1 (Ps1) are regulated by methylation and also that low levels of folate and vitamin B12 in culture medium can cause a reduction of SAM levels, and a consequent increase in PS1 and BACE levels with increased Aβ peptide production. In an experimental model, folate-deficient diet supplemented by Hcy decreased SAM concentration and SAM/SAH ratio in both placenta and liver of pregnant rats, and these changes were linked to a decrease in DNA methylation [33]. Based on these studies, we developed an experimental model to evaluate the effects of maternal vitamin B deficiency on offspring programming of genes involved in AD predisposition.…”

Section: Discussionmentioning

confidence: 99%

Maternal Vitamin B Deficiency and Epigenetic Changes of Genes Involved in the Alzheimer’ s Disease Pathogenesis

Silva¹,

Fernandes²,

Agamme³

et al. 2017

Biol Med (Aligarh)

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Alzheimer's disease (AD) is characterized by progressive neurodegenerative impairment of the central nervous system and is the most prevalent form of dementia. Considering the influence of maternal nutrition on fetal programming, which consequences usually come later in life, we investigated whether maternal vitamin B deficiency during early development alters the offspring expression of genes related to AD etiopathogenesis. Mice dams were submitted to experimental diet one month before and during pregnancy or pregnancy/lactation and, after birth, their offspring were distributed into three groups: control "CT", deficient pregnancy "DP" and deficient pregnancy and lactation "DPL". At postnatal day (PND) 0, a significant decrease of App in females (p=0.007) and App and Bace1 in males (p=0.030 and p=0.040, respectively) was observed when compared to CT group. At PND 28, DPL female presented an increase of App, Bace1 and Ps1 gene expression when compared to CT (p=0.003, p=0.003 and p=0.002, respectively) and DP groups (p=0.017, p=0.005 and p=0.002, respectively). In males at PND 28, a decrease of App and Ps1 was observed in both DP (p=0.012; p=0.001) and DPL (p=0.001; p=0.04) when compared to CT group. No differences were observed in females and males at PND 210. Regarding APP, BACE1 and PS1 protein expression and global DNA methylation pattern, no difference was observed throughout development in female or male offspring. Regarding behavioral evaluations, no changes were observed in the object recognition task, but the DPL males presented lower locomotor activity when compared to DP (p=0.028) and CT (p=0.003) groups. In conclusion, the early exposition to vitamin B deficiency alters the expression of genes related to AD.

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“…(Burdge & Lillycrop, 2010) for review). Further, several studies have reported that altered maternal intake of folate is linked to change of DNA methylation in the offspring (Kim, et al, 2009;Waterland, et al, 2006;Waterland & Jirtle, 2003). Folate deficiency has been strongly associated with incomplete closure of the neural tube.…”

Section: Role Of Maternal Dietmentioning

confidence: 99%

DNA methylation in development

Pan¹,

Smith²,

Zakár³

2012

Embryology - Updates and Highlights on Classic Topics

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Effect of folate deficiency on placental DNA methylation in hyperhomocysteinemic rats

Cited by 84 publications

References 29 publications

The Placenta as a Mediator of Stress Effects on Neurodevelopmental Reprogramming

The Placenta as a Mediator of Stress Effects on Neurodevelopmental Reprogramming

Maternal Vitamin B Deficiency and Epigenetic Changes of Genes Involved in the Alzheimer’ s Disease Pathogenesis

DNA methylation in development

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