Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA314946 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Sex difference had been implicated in pathophysiology and prognosis of common diseases, such as acute lymphoblastic leukemia and coronary heart disease. It is well known that the disease phenotype is shaped by the interaction between the environment, genome, and epigenome. The environmental and the genetic components were extensively studied in the past. Unlike the formers, the role of epigenetics has only been recently investigated. To date, little has been known about differences in epigenetic makeup between the two sexes. Here we present a genome-wide study of sex-specific differences in DNA methylation in healthy individuals. We compared the methylation status of ~26,000 CpGs in the promoter of ~14,000 genes between age-matched males (n=12) and females (n=12). We identified 19 CpGs in 18 genes to have significant sex-specific methylation differences. Our finding was validated by a recent publication of Liu et al. 2010 where they found similar results (ie. 11 of their 12 CpGs overlapped with ours) using the same microarray platform. However, with further investigation we showed that the probes with sex-specific methylation differences displayed cross-reactive targets on the sex chromosomes. This data indicates that autosomal sex-specific methylation detected in this study and by Lui et al, 2010 using the Illumina array platform, is the result of technical artifacts or non-specificity of those microarray probes. Overall, our findings suggest that there is no sex-specific DNA methylation difference in human beyond the sex chromosomes using the Illumina Methylation 27 microarray. Genome-wide DNA methylation data of sodium-bisulfite converted-genomic DNA obtained from whole blood lymphocytes of 12 healthy males compared to that of 12 age-matched healthy females
2011-08-21 | E-GEOD-23638 | biostudies-arrayexpress
Project description:Samples from 43 AD patients and 30 age-matched normal controls were assayed using Illumina© Infinium MethylationEPIC BeadChip. The epigenome-wide association study (EWAS) was performed to evaluate the epigenetic differences using granulocyte and monocyte samples. LOY status of each individual was taken into account when performing differential methylation analyses.
2024-02-01 | GSE226298 | GEO
Project description:Sex difference had been implicated in pathophysiology and prognosis of common diseases, such as acute lymphoblastic leukemia and coronary heart disease. It is well known that the disease phenotype is shaped by the interaction between the environment, genome, and epigenome. The environmental and the genetic components were extensively studied in the past. Unlike the formers, the role of epigenetics has only been recently investigated. To date, little has been known about differences in epigenetic makeup between the two sexes. Here we present a genome-wide study of sex-specific differences in DNA methylation in healthy individuals. We compared the methylation status of ~26,000 CpGs in the promoter of ~14,000 genes between age-matched males (n=12) and females (n=12). We identified 19 CpGs in 18 genes to have significant sex-specific methylation differences. Our finding was validated by a recent publication of Liu et al. 2010 where they found similar results (ie. 11 of their 12 CpGs overlapped with ours) using the same microarray platform. However, with further investigation we showed that the probes with sex-specific methylation differences displayed cross-reactive targets on the sex chromosomes. This data indicates that autosomal sex-specific methylation detected in this study and by Lui et al, 2010 using the Illumina array platform, is the result of technical artifacts or non-specificity of those microarray probes. Overall, our findings suggest that there is no sex-specific DNA methylation difference in human beyond the sex chromosomes using the Illumina Methylation 27 microarray.
2011-08-22 | GSE23638 | GEO
Project description:Samples from 72 AD patients and 62 age-matched cognitively normal controls were assayed using Illumina© Infinium MethylationEPIC BeadChip. We performed an epigenome-wide association study (EWAS) to evaluate the epigenetic differences using post-mortem superior temporal gyrus (STG) and inferior frontal gyrus (IFG) samples. We performed an epigenome-wide association study (EWAS) to evaluate the epigenetic differences using post-mortem superior temporal gyrus (STG) and inferior frontal gyrus (IFG) samples.
2020-10-20 | GSE156984 | GEO
Project description:Human DNA methylation Beadchip v1.2 was used to profile n=310 whole blood samples. The main goal of the study was to measure the epigenetic age (also known as DNA methylation age) of different ethnic groups. Here we focus on subjects older than 35. Groups include Tsimane Indians, Hispanics, and Caucasian samples. To measure DNA methylation age, we used the epigenetic clock software described in Horvath S (n=2013) DNA methylation age of human tissues and cell types. Genome Biology.2013, 14:R115. DOI: 10.1186/10.1186/gb-2013-14-10-r115 PMID: 24138928.
2016-07-13 | GSE72773 | GEO
Project description:Human DNA methylation Beadchip v1.2 was used to profile n=46 whole blood samples. The main goal of the study was to measure the epigenetic age (also known as DNA methylation age) of different ethnic groups. Here we focus on subjects younger than 35 years old. Groups include Tsimane Indians and Caucasian samples. To measure DNA methylation age, we used the epigenetic clock software described in Horvath S (n=2013) DNA methylation age of human tissues and cell types. Genome Biology.2013, 14:R115. DOI: 10.1186/10.1186/gb-2013-14-10-r115 PMID: 24138928.
2016-07-13 | GSE72777 | GEO
Project description:In this epigenome-wide association study (EWAS), we examined the associations between PCDD, PCDF, and PCB exposures and DNA methylation. Whole blood DNA methylation was measured using Illumina EPIC arrays (n=292). We modeled lipid-adjusted toxic equivalencies (TEQs) for: ΣDioxins (sum of 28 PCDDs, PCDFs, cPCBs, and mPCBs), PCDDs, PCDFs, cPCBs, and mPCBs using robust multivariable linear regression adjusting for age, race, sex, smoking, total lipids, and estimated percentages of six blood cell types.
2023-04-23 | GSE149412 | GEO
Project description:Genome wide DNA methylation assays was conducted using the Illumina Infinium MethylationEPIC BeadArray technology (Methyl850K chip) that allows genome-wide DNA methylation analysis of 866,836 CpG sites. We included baseline and 2-year follow-up samples from 25 persons with mild cognitive impairment (cases) and 20 persons with cognitively normal (controls). Sample was balanced by age and sex.
2021-12-10 | GSE190540 | GEO
Project description:Type 2 diabetes (T2D) is among the leading causes of death in the U.S. Ethnic differences in T2D prevalence are evident, including especially for Native Hawaiians (NHs) who remain disproportionately affected by it. This difference in T2D susceptibility involves an interplay between genetic and environmental factors, of which epigenetic mechanisms, including DNA methylation (DNAm) provide a novel approach to investigating gene-environment interactions of health and disease. Monocytes, an innate immune cell intrinsic to the inflammatory response, are a fundamental immune cell component that likely underlies T2D pathogenesis, given their involvement in inflammation and inflammation-associated insulin resistance and metabolic dysfunction. From participants enrolled into the Multiethnic Cohort Study (MEC), who self-identified as NH (n=152), Japanese American (JA; n=119), or White (n=121), we investigated monocyte-specific DNAm patterns in participants at a baseline visit, when free of T2D, using the HumanMethylation850K (850K) to determine whether monocytes harbor an ethnic-specific epigenetic signature of T2D risk that precedes T2D diagnosis. Using an epigenome-wide association study (EWAS), we found 904 significantly (q < 0.01) differentially methylated loci (DML) at a 5% difference in DNAm between participants who remained T2D free at a 15-year follow-up (i.e., controls) and those that would be diagnosed with T2D by follow-up (i.e., incident T2D) after adjusted for age, sex, and education level. These methylation differences were enriched at regulatory regions of the genome, including intergenic and intragenic regions. Notably, these DML were able to distinctly stratify NHs by T2D risk groups, however, this signature was inapparent in Whites and JAs. Likewise, NHs in the incident T2D group displayed a higher degree of DNAm variability. Sensitivity analysis with traditional risk factors (fasting glucose and body mass index [BMI]) and neighborhood socioeconomic status (nSES) found these risk factors had minimal effect on T2D risk-associated DML. Next, using a similar approach we found ethnic-specific DML in monocytes that was able to uniquely stratify NHs, JAs, and Whites, however, in NHs this epigenetic landscape displayed a higher degree of DNAm variability. Similarly, these DML were enriched at regulatory regions of the genome. In both cases, we found genes associated with biological functions and pathways relevant to monocyte functionality, including immune activation and cellular metabolism. Due to the higher degree of epigenetic variability in NHs, including especially NHs with T2D risk, we investigated differentially variable CpGs associated with T2D risk and ethnic-differences. We found differentially variable CpGs between T2D risk groups were able to stratify NHs with and without T2D risk, whereas it was unresolvable in JAs and Whites. Ethnic-specific DNAm variability clustered each ethnic population distinctly, and NH controls were further partitioned from NHs with T2D risk. Our findings suggest monocytes harbor a unique DNAm signature associated with T2D risk, which may be related to ethnic differences that underlie DNAm variability in monocytes. The increased epigenetic variability in monocytes from NHs may underlie epigenetic plasticity that could allow these cells to readily respond to adverse environmental conditions throughout the life course that may underlie long-term disease risk, whereas in other less susceptible populations with similar environmental exposure, this epigenetic plasticity may not be apparent in monocytes.
2024-06-22 | GSE270223 | GEO
Project description:Kidney miRNA expression was examined in F344 rats at 2, 5, 6, 8, 15, 21, 78, and 104 weeks of age in both sexes using Agilent miRNA microarrays. 311 miRNAs were found to be expressed in at least one age and sex. Filtering criteria of ≥1.5 fold change and ANOVA (FDR <5%) revealed 174 differentially expressed miRNAs in the kidney; 173 and 34 miRNAs exhibiting age and sex effects, respectively. Principal component analysis revealed age effects predominated over sex effects, with 2 week miRNA expression being much different from other ages. No significant sexually dimorphic miRNA expression was observed from 5 to 8 weeks, while the most differential expression (13 miRNAs) was observed at 21 weeks. Potential target genes of these differentially expressed miRNAs were identified. Pathway analysis was used to investigate the possible roles of these target genes in age- and sex-specific differences.
2015-01-10 | GSE64842 | GEO