Select Early-Life Environmental Exposures and DNA Methylation in the Placenta

Mortillo, Michael; Marsit, Carmen J.

doi:10.1007/s40572-022-00385-1

Cited by 19 publications

(11 citation statements)

References 98 publications

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“…Several studies have also focused on using placental ‘omics to gain mechanistic insight into the relationship between the in utero environment and birth outcomes such as fetal growth, preterm delivery, and birthweight, and infant and childhood health outcomes such as neurocognition and behavior [ 81 , 82 ]. As observed in our study from prenatal cannabis exposure, dysregulation of placental DNA methylation (DNAm) in response to the in utero environment is a common finding [ 81 ]. A prior literature review that included studies of placental DNAm and/or transcriptomics in response to the prenatal environment identified 28 articles meeting their search criteria.…”

Section: Discussionmentioning

confidence: 99%

Prenatal delta-9-tetrahydrocannabinol exposure is associated with changes in rhesus macaque DNA methylation enriched for autism genes

et al. 2023

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Background With the growing availability of cannabis and the popularization of additional routes of cannabis use beyond smoking, including edibles, the prevalence of cannabis use in pregnancy is rapidly increasing. However, the potential effects of prenatal cannabis use on fetal developmental programming remain unknown. Results We designed this study to determine whether the use of edible cannabis during pregnancy is deleterious to the fetal and placental epigenome. Pregnant rhesus macaques consumed a daily edible containing either delta-9-tetrahydrocannabinol (THC) (2.5 mg/7 kg/day) or placebo. DNA methylation was measured in 5 tissues collected at cesarean delivery (placenta, lung, cerebellum, prefrontal cortex, and right ventricle of the heart) using the Illumina MethylationEPIC platform and filtering for probes previously validated in rhesus macaque. In utero exposure to THC was associated with differential methylation at 581 CpGs, with 573 (98%) identified in placenta. Loci differentially methylated with THC were enriched for candidate autism spectrum disorder (ASD) genes from the Simons Foundation Autism Research Initiative (SFARI) database in all tissues. The placenta demonstrated greatest SFARI gene enrichment, including genes differentially methylated in placentas from a prospective ASD study. Conclusions Overall, our findings reveal that prenatal THC exposure alters placental and fetal DNA methylation at genes involved in neurobehavioral development that may influence longer-term offspring outcomes. The data from this study add to the limited existing literature to help guide patient counseling and public health polices focused on prenatal cannabis use in the future.

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Section: Discussionmentioning

confidence: 99%

Prenatal delta-9-tetrahydrocannabinol exposure is associated with changes in rhesus macaque DNA methylation enriched for autism genes

et al. 2023

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“…17 Environmental factors in the prenatal period influence the process of DNA methylation of placental cells and alter gene expression. 18 Methylated histones can be maintained during cell division, and the complex responsible for methylation of histone H3 on lysine 27 can be fixed on chromatin by DNA replication and passed down through generations. Additionally, the process of RNA interference plays an important role in the regulation of gene expression and influences enzymes that modify histones and binding proteins.…”

Section: Epigenetic Theories On the Development Of Metsmentioning

confidence: 99%

(Epi)genetic Aspects of Metabolic Syndrome Pathogenesis in Relation to Brain-derived Neurotrophic Factor Expression: A Review

Todosenko,

Yurova,

Khaziakhmatova

et al. 2024

Gene Expr

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A key element in the pathogenesis of metabolic syndrome (MetS) is the reprogramming of hypothalamic cells at the genetic level (in the prenatal phase), which leads to neuroinflammation. We hypothesize that alterations in the structure of hypothalamic neurons mediated by (epi)genetic alterations are directly related to impaired expression/production of neurotrophins and neurotransmitters that control the metabolism of substances in the brain and periphery, including brain-derived neurotrophic factor (BDNF). The aim of this review is to describe the molecular genetic and epigenetic role of BDNF in the development of MetS. Articles entered into the National Library of Medicine Medline database via the PubMed interface were used to create this review. We attempted to include as much literature as possible, including reviews, animal studies, cell culture studies, and clinical trials. Studies on BDNF point to its role in metabolic processes, including glucose, insulin, and cholesterol homeostasis. Evidence-based studies show that multiple genes in close proximity to BDNF are involved in the development of MetS. Studies aimed at analyzing BDNF in metabolic diseases using different biological samples will reveal clear pathophysiological links

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“…Studies in hypertensive rat models have further indicated a direct association between hypertension and hypermethylation of HSD11B2 ( 65 ). Moreover, in newborns, hypermethylation of the HSD11B2 gene, coupled with reduced HSD11B2 mRNA levels, suggests a potential mechanism for EH through abnormal renal sodium reabsorption ( 66 – 68 ).…”

Section: Interaction Between Epigenetics and Hypertensionmentioning

confidence: 99%

Epigenetics of hypertension as a risk factor for the development of coronary artery disease in type 2 diabetes mellitus

Karabaeva,

Vochshenkova,

Mussin

et al. 2024

Front. Endocrinol.

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Hypertension, a multifaceted cardiovascular disorder influenced by genetic, epigenetic, and environmental factors, poses a significant risk for the development of coronary artery disease (CAD) in individuals with type 2 diabetes mellitus (T2DM). Epigenetic alterations, particularly in histone modifications, DNA methylation, and microRNAs, play a pivotal role in unraveling the complex molecular underpinnings of blood pressure regulation. This review emphasizes the crucial interplay between epigenetic attributes and hypertension, shedding light on the prominence of DNA methylation, both globally and at the gene-specific level, in essential hypertension. Additionally, histone modifications, including acetylation and methylation, emerge as essential epigenetic markers linked to hypertension. Furthermore, microRNAs exert regulatory influence on blood pressure homeostasis, targeting key genes within the aldosterone and renin-angiotensin pathways. Understanding the intricate crosstalk between genetics and epigenetics in hypertension is particularly pertinent in the context of its interaction with T2DM, where hypertension serves as a notable risk factor for the development of CAD. These findings not only contribute to the comprehensive elucidation of essential hypertension but also offer promising avenues for innovative strategies in the prevention and treatment of cardiovascular complications, especially in the context of T2DM.

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Select Early-Life Environmental Exposures and DNA Methylation in the Placenta

Cited by 19 publications

References 98 publications

Prenatal delta-9-tetrahydrocannabinol exposure is associated with changes in rhesus macaque DNA methylation enriched for autism genes

Prenatal delta-9-tetrahydrocannabinol exposure is associated with changes in rhesus macaque DNA methylation enriched for autism genes

(Epi)genetic Aspects of Metabolic Syndrome Pathogenesis in Relation to Brain-derived Neurotrophic Factor Expression: A Review

Epigenetics of hypertension as a risk factor for the development of coronary artery disease in type 2 diabetes mellitus

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