scholarly journals The effect of season of birth on brain epigenome-wide DNA methylation of older adults

2021 ◽  
pp. 1-11
Author(s):  
Altug Didikoglu ◽  
Nisha Nair ◽  
Andrew C. Robinson ◽  
Federico Roncaroli ◽  
Neil Pendleton ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Human Brain ◽  
Neural Development ◽  
Statistical Power ◽  
Clock Genes ◽  
Light Exposure ◽  
Temporal Cortex ◽  
Later Life ◽  
Methylation Profile ◽  
Season Of Birth

Abstract Perinatal light exposure predisposes towards health and behaviour in adulthood. Season of birth is associated with psychiatric, allergic, cardiovascular and metabolic problems. It has been proposed that early-life environmental light disrupts the development of biological rhythms which, in turn, influence later-life health. However, the mechanisms linking perinatal seasonal light to later-life biological rhythm and health in humans are unknown. In this study, we investigated the association between season of birth and epigenome-wide DNA methylation of two postmortem human brain regions (16 hypothalamus, 14 temporal cortex). We did not find statistically significant differences at the whole epigenome level, either because we lacked statistical power or that no association exists. However, when we examined 24 CpG sites that had the highest significance or differential methylation, we identified regions which may be associated with circadian rhythm entrainment, cholinergic neurotransmission and neural development. Amongst methylation of the core clock genes, we identified that hypothalamus Neuronal PAS Domain Protein 2 (NPAS2) gene has hypermethylated regions in long photoperiod-born individuals. In addition, we found nominal associations between season of birth and genes linked to chronotype and narcolepsy. Season of birth-related brain DNA methylation profile was different than a previously reported blood methylation profile, suggesting a tissue-specific mechanism of perinatal light programming. Overall, we are the first to analyse the relationship between season of birth and human brain DNA methylation. Further studies with larger sample sizes are required to confirm an imprinting effect of perinatal light on the circadian clock.

Epigenetic Mechanisms of Maternal Dietary Protein and Amino Acids Affecting Growth and Development of Offspring

2019 ◽  
Vol 20 (7) ◽  
pp. 727-735 ◽  
Author(s):  
Yi Wu ◽  
Zhibin Cheng ◽  
Yueyu Bai ◽  
Xi Ma
Keyword(s):  
Amino Acids ◽  
Dna Methylation ◽  
Dietary Protein ◽  
Growth And Development ◽  
Later Life ◽  
Biological Macromolecules ◽  
Epigenetic Mechanisms ◽  
Maternal Circulation ◽  
Energy Processing ◽  
Living Organisms

Nutrients can regulate metabolic activities of living organisms through epigenetic mechanisms, including DNA methylation, histone modification, and RNA regulation. Since the nutrients required for early embryos and postpartum lactation are derived in whole or in part from maternal and lactating nutrition, the maternal nutritional level affects the growth and development of fetus and creates a profound relationship between disease development and early environmental exposure in the offspring’s later life. Protein is one of the most important biological macromolecules, involved in almost every process of life, such as information transmission, energy processing and material metabolism. Maternal protein intake levels may affect the integrity of the fetal genome and alter DNA methylation and gene expression. Most amino acids are supplied to the fetus from the maternal circulation through active transport of placenta. Some amino acids, such as methionine, as dietary methyl donor, play an important role in DNA methylation and body’s one-carbon metabolism. The purpose of this review is to describe effects of maternal dietary protein and amino acid intake on fetal and neonatal growth and development through epigenetic mechanisms, with examples in humans and animals.

scholarly journals Integrated analysis of DNA methylation profile in HLA-G gene and imaging in coronary heart disease

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
G Benincasa ◽  
C Schiano ◽  
T Infante ◽  
M Franzese ◽  
R Casale ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Coronary Heart Disease ◽  
Heart Disease ◽  
Cpg Island ◽  
Methylation Profile ◽  
Integrated Analysis ◽  
Funding Source ◽  
Relevant Parameter ◽  
Cardiac Computed Tomography Angiography ◽  
Dna Methylation Profile

Abstract Aims Immune endothelial inflammation, underlie coronary heart disease (CHD) related phenotypes, could provide new insight into the pathobiology of the disease. We investigated DNA methylation level of the unique CpG island of HLA-G gene in CHD patients and evaluated the correlation with cardiac computed tomography angiography (CCTA) features. Methods Thirty-two patients that underwent CCTA for suspected CHD were enrolled for this study. Obstructive CHD group included fourteen patients, in which there was a stenosis greater than or equal to 50% in one or more of the major coronary arteries detected; whereas subjects with Calcium (Ca) Score=0, uninjured coronaries and with no obstructive CHD were considered as control subjects (Ctrls) (n=18). For both groups, DNA methylation profile of the whole 5'UTR-CpG island of HLA-G was measured. The plasma soluble HLA-G (sHLA-G) levels were detected in all subjects by specific ELISA assay. Statistical analysis was performed using R software. Results For the first time, our study reported that 1) a significant hypomethylation characterized three specific fragments (B, C and F) of the 5'UTR-CpG island (p=0.05) of HLA-G gene in CHD patients compared to Ctrl group; 2) hypomethylation level of one specific fragment positively correlated with coronary Ca score, a relevant parameter of CCTA (p<0.05) between two groups. Conclusions Our results showed that reduced levels of circulating HLA-G molecules could derive from epigenetic marks inducing hypomethylation of specific regions into 5'UTR-CpG island of HLA-G gene in CHD patients with obstructive coronary stenosis vs non critical stenosis group. Funding Acknowledgement Type of funding source: Public grant(s) – National budget only. Main funding source(s): Italian Minister of Health

098 Effects of Metameric Display-Light on Alertness, Vigilance and Melatonin

SLEEP ◽  
2021 ◽  
Vol 44 (Supplement_2) ◽  
pp. A40-A41
Author(s):  
Isabel Schöllhorn ◽  
Oliver Stefani ◽  
Manuel Spitschan ◽  
Robert Lucas ◽  
Christian Cajochen
Keyword(s):  
Statistical Power ◽  
Light Exposure ◽  
Vigilance Task ◽  
Ongoing Study ◽  
Swiss National Science Foundation ◽  
Visual Appearance ◽  
Salivary Melatonin ◽  
Subjective Alertness ◽  
Psychomotor Vigilance ◽  
Circadian Physiology

Abstract Introduction Light emitted from visual displays can acutely increase alertness, improve cognitive performance and suppress melatonin in the evening. Here we tested the influence of different melanopic irradiance levels emitted by a metameric display setting on alertness, vigilance and salivary melatonin levels. Methods In an ongoing study, 37 healthy, male participants have so far completed a 2-week study protocol. Volunteers were assigned to one of four luminance groups which differed in brightness levels (27 cd/m2 - 280 cd/m2). Illuminance ranged between 7 and 85 lx. Within the four groups each volunteer was exposed to a low melanopic (LM) and a high melanopic condition (HM). The LM and HM differed in melanopic irradiance (ca. 3-fold change), but matched in terms of cone excitation (metamers). Before, during and after the light exposure, volunteers performed a psychomotor vigilance task (PVT). Subjective alertness and melatonin levels were continuously measured in half-hourly intervals throughout scheduled wakefulness in the 17-h in lab study. Results Preliminary analysis yielded an overall alerting response in the HM vs. the LM condition (p<0.05) concomitant with a trend of reduced melatonin levels in HM vs. LM (p=0.08). So far, we could not observe a difference in PVT performance for HM and LM (Reaction time responses between 100 and 500 ms). Since we are still lacking statistical power in the ongoing study, we cannot yet satisfactorily interpret interaction effects between melanopic condition and brightness. Conclusion Our data indicate that rather low brightness levels of high melanopic display light impacts alertness and melatonin levels in the evening. Thus, metameric low melanopic display light may be a promising method to attenuate activating properties of evening light on circadian physiology without affecting visual appearance. Support (if any) This project is funded by the Swiss National Science Foundation (SNSF).

scholarly journals DNA methylation patterns identify subgroups of pancreatic neuroendocrine tumors with clinical association

2021 ◽  
Vol 4 (1) ◽  
Author(s):  
Vanessa Lakis ◽  
◽  
Rita T. Lawlor ◽  
Felicity Newell ◽  
Ann-Marie Patch ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Neuroendocrine Tumors ◽  
Methylation Profile ◽  
Pancreatic Neuroendocrine Tumors ◽  
Wild Type ◽  
Genomic Information ◽  
Chromosome 11 ◽  
Dna Methylation Profile ◽  
Methylation Patterns ◽  
Recurrent Patterns

AbstractHere we report the DNA methylation profile of 84 sporadic pancreatic neuroendocrine tumors (PanNETs) with associated clinical and genomic information. We identified three subgroups of PanNETs, termed T1, T2 and T3, with distinct patterns of methylation. The T1 subgroup was enriched for functional tumors and ATRX, DAXX and MEN1 wild-type genotypes. The T2 subgroup contained tumors with mutations in ATRX, DAXX and MEN1 and recurrent patterns of chromosomal losses in half of the genome with no association between regions with recurrent loss and methylation levels. T2 tumors were larger and had lower methylation in the MGMT gene body, which showed positive correlation with gene expression. The T3 subgroup harboured mutations in MEN1 with recurrent loss of chromosome 11, was enriched for grade G1 tumors and showed histological parameters associated with better prognosis. Our results suggest a role for methylation in both driving tumorigenesis and potentially stratifying prognosis in PanNETs.

scholarly journals Common genetic variants with fetal effects on birth weight are enriched for proximity to genes implicated in rare developmental disorders

2021 ◽  
Author(s):  
Robin N Beaumont ◽  
Isabelle K Mayne ◽  
Rachel M Freathy ◽  
Caroline F Wright
Keyword(s):  
Birth Weight ◽  
Statistical Power ◽  
Developmental Disorders ◽  
Association Studies ◽  
Later Life ◽  
Genome Wide Association Studies ◽  
Nucleotide Polymorphisms ◽  
Genome Wide ◽  
Common Genetic Variants ◽  
Causal Genes

Abstract Birth weight is an important factor in newborn survival; both low and high birth weights are associated with adverse later-life health outcomes. Genome-wide association studies (GWAS) have identified 190 loci associated with maternal or fetal effects on birth weight. Knowledge of the underlying causal genes is crucial to understand how these loci influence birth weight and the links between infant and adult morbidity. Numerous monogenic developmental syndromes are associated with birth weights at the extreme ends of the distribution. Genes implicated in those syndromes may provide valuable information to prioritize candidate genes at the GWAS loci. We examined the proximity of genes implicated in developmental disorders (DDs) to birth weight GWAS loci using simulations to test whether they fall disproportionately close to the GWAS loci. We found birth weight GWAS single nucleotide polymorphisms (SNPs) fall closer to such genes than expected both when the DD gene is the nearest gene to the birth weight SNP and also when examining all genes within 258 kb of the SNP. This enrichment was driven by genes causing monogenic DDs with dominant modes of inheritance. We found examples of SNPs in the intron of one gene marking plausible effects via different nearby genes, highlighting the closest gene to the SNP not necessarily being the functionally relevant gene. This is the first application of this approach to birth weight, which has helped identify GWAS loci likely to have direct fetal effects on birth weight, which could not previously be classified as fetal or maternal owing to insufficient statistical power.

scholarly journals A Genome-Wide Integrative Association Study of DNA Methylation and Gene Expression Data and Later Life Cognitive Functioning in Monozygotic Twins

2020 ◽  
Vol 14 ◽  
Author(s):  
Mette Soerensen ◽  
Dominika Marzena Hozakowska-Roszkowska ◽  
Marianne Nygaard ◽  
Martin J. Larsen ◽  
Veit Schwämmle ◽  
...  
Keyword(s):  
Gene Expression ◽  
Dna Methylation ◽  
Cognitive Functioning ◽  
Association Study ◽  
Gene Expression Data ◽  
Monozygotic Twins ◽  
Later Life ◽  
Expression Data ◽  
Genome Wide ◽  
A Genome

scholarly journals DNA methylation profile of genes involved in inflammation and autoimmunity correlates with vascular function in morbidly obese adults

Epigenetics ◽  
2021 ◽  
pp. 1-17
Author(s):  
Mohamed M. Ali ◽  
Dina Naquiallah ◽  
Maryam Qureshi ◽  
Mohammed Imaduddin Mirza ◽  
Chandra Hassan ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Vascular Function ◽  
Methylation Profile ◽  
Morbidly Obese ◽  
Obese Adults ◽  
Dna Methylation Profile

Overlapping DNA methylation profile between placentas with trisomy 16 and early-onset preeclampsia

Placenta ◽  
2014 ◽  
Vol 35 (3) ◽  
pp. 216-222 ◽  
Author(s):  
J.D. Blair ◽  
S. Langlois ◽  
D.E. McFadden ◽  
W.P. Robinson
Keyword(s):  
Dna Methylation ◽  
Early Onset ◽  
Methylation Profile ◽  
Trisomy 16 ◽  
Dna Methylation Profile ◽  
Early Onset Preeclampsia

scholarly journals Genome-Wide DNA Methylation Pattern of Cancer Stem Cells in Esophageal Cancer

2020 ◽  
Vol 19 ◽  
pp. 153303382098379
Author(s):  
Xiying Yu ◽  
Ying Teng ◽  
Xingran Jiang ◽  
Hui Yuan ◽  
Wei Jiang
Keyword(s):  
Dna Methylation ◽  
Stem Cells ◽  
Esophageal Cancer ◽  
Cancer Stem Cells ◽  
Side Population ◽  
Methylation Status ◽  
Methylation Profile ◽  
Cpg Dinucleotides ◽  
Genome Wide ◽  
Differentially Methylated Genes

Background: Cancer stem cells (CSCs) are considered the main cause of cancer recurrence and metastasis, and DNA methylation is involved in the maintenance of CSCs. However, the methylation profile of esophageal CSCs remains unknown. Methods: Side population (SP) cells were isolated from esophageal squamous cell carcinoma (ESCC) cell lines KYSE150 and EC109. Sphere-forming cells were collected from human primary esophageal cancer cells. SP cells and sphere-forming cells were used as substitutes for cancer stem-like cells. We investigated the genome-wide DNA methylation profile in esophageal cancer stem-like cells using reduced representation bisulfite sequencing (RRBS). Results: Methylated cytosine (mC) was found mostly in CpG dinucleotides, located mostly in the intronic, intergenic, and exonic regions. Forty intersected differentially methylated regions (DMRs) were identified in these 3 groups of samples. Thirteen differentially methylated genes with the same alteration trend were detected; these included OTX1, SPACA1, CD163L1, ST8SIA2, TECR, CADM3, GRM1, LRRK1, CHSY1, PROKR2, LINC00658, LOC100506688, and NKD2. DMRs covering ST8SIA2 and GRM1 were located in exons. These differentially methylated genes were involved in 10 categories of biological processes and 3 cell signaling pathways. Conclusions: When compared to non-CSCs, cancer stem-like cells have a differential methylation status, which provides an important biological base for understanding esophageal CSCs and developing therapeutic targets for esophageal cancer.

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