Impact of vitamin D depletion during development on mouse sperm DNA methylation

Xue, Jing; Gharaibeh, Raad Z.; Pietryk, Edward W.; Brouwer, Cory; Tarantino, Lisa M.; Valdar, William; Ideraabdullah, Folami Y.

doi:10.1080/15592294.2018.1526027

Cited by 13 publications

(8 citation statements)

References 51 publications

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“…In addition, maternal plasma levels of vitamin D along with ancestry affect DNA methylation in infants [219]. Murine models showed that vitamin D deficiency during pre-and postnatal development induces changes in the methylome that can persist throughout many generations [220,221]. More specifically, maternal vitamin D status, as well as gestational supplementation with this micronutrient, inversely correlate with perinatal DNA methylation at the retinoid X receptor alpha (RXRA) gene [222,223].…”

Section: Vitaminsmentioning

confidence: 99%

Perinatal and Early-Life Nutrition, Epigenetics, and Allergy

et al. 2021

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Epidemiological studies have shown a dramatic increase in the incidence and the prevalence of allergic diseases over the last several decades. Environmental triggers including risk factors (e.g., pollution), the loss of rural living conditions (e.g., farming conditions), and nutritional status (e.g., maternal, breastfeeding) are considered major contributors to this increase. The influences of these environmental factors are thought to be mediated by epigenetic mechanisms which are heritable, reversible, and biologically relevant biochemical modifications of the chromatin carrying the genetic information without changing the nucleotide sequence of the genome. An important feature characterizing epigenetically-mediated processes is the existence of a time frame where the induced effects are the strongest and therefore most crucial. This period between conception, pregnancy, and the first years of life (e.g., first 1000 days) is considered the optimal time for environmental factors, such as nutrition, to exert their beneficial epigenetic effects. In the current review, we discussed the impact of the exposure to bacteria, viruses, parasites, fungal components, microbiome metabolites, and specific nutritional components (e.g., polyunsaturated fatty acids (PUFA), vitamins, plant- and animal-derived microRNAs, breast milk) on the epigenetic patterns related to allergic manifestations. We gave insight into the epigenetic signature of bioactive milk components and the effects of specific nutrition on neonatal T cell development. Several lines of evidence suggest that atypical metabolic reprogramming induced by extrinsic factors such as allergens, viruses, pollutants, diet, or microbiome might drive cellular metabolic dysfunctions and defective immune responses in allergic disease. Therefore, we described the current knowledge on the relationship between immunometabolism and allergy mediated by epigenetic mechanisms. The knowledge as presented will give insight into epigenetic changes and the potential of maternal and post-natal nutrition on the development of allergic disease.

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Section: Vitaminsmentioning

confidence: 99%

Perinatal and Early-Life Nutrition, Epigenetics, and Allergy

et al. 2021

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“…The ZNF232 locus was associated with a family history of Alzheimer’s disease in a GWA meta-analysis [93]. The intergenic CpG on chromosome 4 (cg27284194) has been previously associated with infertility [94,95]. In GWASs, the region 4: 927973–1039876 (harboring mQTLs for cg27284194) has been associated with a number of traits and diseases, including bone mineral density [96,97,98,99,100] and several metabolomic characteristics such as blood protein [101,102] and triglyceride [103] levels (See Table S19).…”

Section: Resultsmentioning

confidence: 99%

DNA Methylation Signatures of Breastfeeding in Buccal Cells Collected in Mid-Childhood

et al. 2019

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Breastfeeding has long-term benefits for children that may be mediated via the epigenome. This pathway has been hypothesized, but the number of empirical studies in humans is small and mostly done by using peripheral blood as the DNA source. We performed an epigenome-wide association study (EWAS) in buccal cells collected around age nine (mean = 9.5) from 1006 twins recruited by the Netherlands Twin Register (NTR). An age-stratified analysis examined if effects attenuate with age (median split at 10 years; n<10 = 517, mean age = 7.9; n>10 = 489, mean age = 11.2). We performed replication analyses in two independent cohorts from the NTR (buccal cells) and the Avon Longitudinal Study of Parents and Children (ALSPAC) (peripheral blood), and we tested loci previously associated with breastfeeding in epigenetic studies. Genome-wide DNA methylation was assessed with the Illumina Infinium MethylationEPIC BeadChip (Illumina, San Diego, CA, USA) in the NTR and with the HumanMethylation450 Bead Chip in the ALSPAC. The duration of breastfeeding was dichotomized (‘never‘ vs. ‘ever’). In the total sample, no robustly associated epigenome-wide significant CpGs were identified (α = 6.34 × 10–8). In the sub-group of children younger than 10 years, four significant CpGs were associated with breastfeeding after adjusting for child and maternal characteristics. In children older than 10 years, methylation differences at these CpGs were smaller and non-significant. The findings did not replicate in the NTR sample (n = 98; mean age = 7.5 years), and no nearby sites were associated with breastfeeding in the ALSPAC study (n = 938; mean age = 7.4). Of the CpG sites previously reported in the literature, three were associated with breastfeeding in children younger than 10 years, thus showing that these CpGs are associated with breastfeeding in buccal and blood cells. Our study is the first to show that breastfeeding is associated with epigenetic variation in buccal cells in children. Further studies are needed to investigate if methylation differences at these loci are caused by breastfeeding or by other unmeasured confounders, as well as what mechanism drives changes in associations with age.

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“…Such paradoxical findings have also been reported in cancer models and suggest that the effects of folate levels on DNA methylation are site-specific rather than epigenome-wide [ 60 , 61 ]. While developmental vitamin D depletion has been generally associated with hypomethylation [ 62 , 63 ], these associations were locus-specific [ 44 ]. Our findings are the first to demonstrate an inverse relationship between developmental vitamin D levels and DNA methylation at MEs.…”

Section: Discussionmentioning

confidence: 99%

Maternal tobacco smoke exposure is associated with increased DNA methylation at human metastable epialleles in infant cord blood

Joglekar

Grenier

Hoyo

et al. 2022

Environmental Epigenetics

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Metastable epialleles (MEs) are genomic regions that are stochastically methylated prior to germ layer specification and exhibit high inter-individual but low intra-individual variability across tissues. ME methylation is vulnerable to environmental stressors, including diet. Tobacco smoke (TS) exposure during pregnancy is associated with adverse impacts on fetal health and maternal micronutrient levels as well as altered methylation. Our objective was to determine if maternal smoke exposure impacts methylation at MEs. Consistent with prior studies, we observed reductions in one carbon-pathway micronutrients with gestational TS exposure, including maternal folate (p=0.02), vitamins B6 (p=0.05), and B12 (p=0.007). We examined putative MEs BOLA3, PAX8, and ZFYVE28 in cord blood specimens from 85 Newborn Epigenetics STudy (NEST) participants. Gestational TS exposure was associated with elevated DNA methylation at PAX8 (+5.22% average methylation; 95% CI: 0.33% to 10.10%; p=0.037). In human conceptal kidney tissues, higher PAX8 transcription was associated with lower methylation (rs=0.55; p=0.07), suggesting that the methylation levels established at MEs, and their environmentally induced perturbation, may have meaningful, tissue-specific functional consequences. This may be particularly important because PAX8 is implicated in several cancers, including pediatric kidney cancer. Our data are the first to indicate vulnerability of human ME methylation establishment to TS exposure, with a general trend of increasing levels of methylation at these loci. Further investigation is needed to determine how TS exposure-mediated changes in DNA methylation at MEs, and consequent expression levels, might affect smoking-related disease risk.

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Impact of vitamin D depletion during development on mouse sperm DNA methylation

Cited by 13 publications

References 51 publications

Perinatal and Early-Life Nutrition, Epigenetics, and Allergy

Perinatal and Early-Life Nutrition, Epigenetics, and Allergy

DNA Methylation Signatures of Breastfeeding in Buccal Cells Collected in Mid-Childhood

Maternal tobacco smoke exposure is associated with increased DNA methylation at human metastable epialleles in infant cord blood

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