Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA141137 | ENA |
REPOSITORIES: ENA
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Project description:Long-term culture associated changes need to be considered for quality control of cell preparations – especially in cellular therapy. Here we describe a simple method to track cellular aging based on continuous DNA-methylation changes at six specific CpG sites. This epigenetic signature can be used as a biomarker for various cell types to predict the state of cellular aging with regard to the number of passages or days of in vitro culture. 8 samples of human dermal fibroblasts. 4 samples of mesenchymal stem cells (MSC) from human adipose tissue.
2012-05-21 | E-GEOD-29661 | biostudies-arrayexpress
Project description:Long-term culture associated changes need to be considered for quality control of cell preparations – especially in cellular therapy. Here we describe a simple method to track cellular aging based on continuous DNA-methylation changes at six specific CpG sites. This epigenetic signature can be used as a biomarker for various cell types to predict the state of cellular aging with regard to the number of passages or days of in vitro culture.
2012-05-22 | GSE29661 | GEO
Project description:Aging is a complex multifactorial process that affects cellular function and tissue homeostasis over time. Despite extensive research, the molecular mechanisms driving cellular aging remain poorly understood. Many studies have focused on changes in DNA methylation as an indicator of aging. In particular, the degree of methylation at polycomb CpG islands has been shown to be predictive of phenotypic changes associated with aging. Since many age-related pathological processes, are thought to be of single-cell origin (e.g. cancer), we questioned whether polycomb DNA methylation also occurs preferentially in a subset of cells within the overall population. Using single-cell whole-genome data from multiple ages and tissues, we identify Average Polycomb CpG Methylation (AvPolyMe) as a hallmark of cellular aging. This revealed that aging occurs at varying rates within specific cells, with proliferating cells showing accelerated levels. Gene expression analysis in “young” and “old” single cells identified changes in immune response, translation regulation, tumorigenesis and other cellular processes associated with aging. These results challenge traditional models of homogeneous cellular aging and suggest that aging is a highly individualized process at the single-cell level that may be driven by programmed changes in polycomb CpG island DNA methylation.
2026-05-05 | GSE290999 | GEO
Project description:Epigenomics is developing a colon cancer screening assay based on differential methylation of specific CpG sites for the detection of early stage disease. A genome-wide methylation analysis and oligonucleotide array study using DNA from various stages of colon cancer and normal tissue have been completed to obtain candidate CpG markers. Based on results obtained in the above studies, Epigenomics has moved to the final stages of feasibility with a specific, highly sensitive real-time marker assay that is able to detect colon cancer DNA in blood plasma.
| 2056787 | ecrin-mdr-crc
Project description:In this study, we have analyzed DNA methylation changes upon long-term culture and aging of MSC by using the HumanMethylation27 BeadChip assessing 27,578 unique CpG sites. Cells were taken from bone marrow aspirates from iliac crest (BM) of healthy donors or from the caput femoris (HIP) of elderly patients that received femoral head prosthesis.Overall, the methylation pattern was maintained throughout both long-term culture and aging but highly significant differences were observed at specific CpG sites. Notably, methylation changes in MSC were related in long-term culture and aging in vivo.
2010-02-04 | GSE17448 | GEO
Project description:Intestinal organoids, three-dimensional cultures from intestinal stem cells, are a powerful model for studying aging, and DNA methylation is an accurate biological clock. Consequently, we hypothesized that organoid DNA methylation could serve as an aging metric and a valuable tool for in vitro aging research. Our initial study revealed significant DNA methylation changes, during organoid culture, with 27% of total CpG sites undergoing hypomethylation, and 11% gaining hypermethylation. Hypomethylation occurred predominantly in aging-associated genomic regions, including non-promoter, non-CpG island regions (e.g., transposable elements), while hypermethylation, in CpG islands, significantly (p < 0.001) correlated with aging. Comparison of aging-methylated sites with differentiation-specific CpG sites showed minimal overlap, indicating negligible association. Early-passage (P0 and P2) organoids, derived from 4- and 24-month-old mice, preserved aging-specific methylation patterns, with a correlation coefficient of 0.48 (p < 0.001) between methylation differences in old versus young primary cells. Conversely, long-term passaging revealed distinct methylation changes, specific to each organoid line. Some early passage organoids exhibited more hypomethylation, clustering with mid-passage (P10 - P13) organoids, while late-passage (P24 and P27) organoids entered a crisis stage with severe hypomethylation, growth arrest, and distant clustering. Transposable elements remained hypomethylated, compared to primary cells. Aging-related methylation sites continued to change with passage, and linear modeling predicted that organoids age at a rate of 0.46 months per week in culture. Treatment with decitabine reversed the methylation age of organoids, derived from 24-month-old mice. These findings suggest that organoids effectively model aging, with further research needed to assess culture-associated influences.
2025-06-01 | GSE294963 | GEO
Project description:Intestinal organoids, three-dimensional cultures from intestinal stem cells, are a powerful model for studying aging, and DNA methylation is an accurate biological clock. Consequently, we hypothesized that organoid DNA methylation could serve as an aging metric and a valuable tool for in vitro aging research. Our initial study revealed significant DNA methylation changes, during organoid culture, with 27% of total CpG sites undergoing hypomethylation, and 11% gaining hypermethylation. Hypomethylation occurred predominantly in aging-associated genomic regions, including non-promoter, non-CpG island regions (e.g., transposable elements), while hypermethylation, in CpG islands, significantly (p < 0.001) correlated with aging. Comparison of aging-methylated sites with differentiation-specific CpG sites showed minimal overlap, indicating negligible association. Early-passage (P0 and P2) organoids, derived from 4- and 24-month-old mice, preserved aging-specific methylation patterns, with a correlation coefficient of 0.48 (p < 0.001) between methylation differences in old versus young primary cells. Conversely, long-term passaging revealed distinct methylation changes, specific to each organoid line. Some early passage organoids exhibited more hypomethylation, clustering with mid-passage (P10 - P13) organoids, while late-passage (P24 and P27) organoids entered a crisis stage with severe hypomethylation, growth arrest, and distant clustering. Transposable elements remained hypomethylated, compared to primary cells. Aging-related methylation sites continued to change with passage, and linear modeling predicted that organoids age at a rate of 0.46 months per week in culture. Treatment with decitabine reversed the methylation age of organoids, derived from 24-month-old mice. These findings suggest that organoids effectively model aging, with further research needed to assess culture-associated influences.
2025-06-01 | GSE295059 | GEO
Project description:The decline of brain function during aging is associated with epigenetic changes, including DNA methylation. Lifestyle interventions can improve brain function during aging, but their influence on age-related epigenetic changes is unknown. Using genome-wide DNA methylation sequencing, we here show that environmental enrichment counteracted age-related DNA methylation changes in the hippocampal dentate gyrus of mice. Specifically, environmental enrichment prevented the aging-induced CpG hypomethylation at target sites of the methyl-CpG-binding protein Mecp2, which is known to control neuronal functions. The genes at which environmental enrichment counteracted aging effects have described roles in neuronal plasticity, neuronal cell communication and adult hippocampal neurogenesis and are dysregulated with age-related cognitive decline in the human brain. Our results highlight the rejuvenating effects of environmental enrichment at the level of DNA methylation and give molecular insights into the specific aspects of brain aging that can be counteracted by lifestyle interventions.
2020-12-31 | GSE138368 | GEO
Project description:In differentiated cells, aging is associated with hypermethylation of DNA regions enriched in repressive histone posttranslational modifications. However, the chromatin marks associated with changes in DNA methylation in adult stem cells during lifetime are still largely unknown. Here, DNA methylation profiling of mesenchymal stem cells obtained from individuals aged 2 to 92 identified 18735 hypermethylated and 45407 hypomethylated CpG sites associated with aging. As in differentiated cells, hypermethylated sequences were enriched in chromatin repressive marks. Most importantly, hypomethylated CpG sites were strongly enriched in the active chromatin mark H3K4me1 in stem and differentiated cells, suggesting this is a cell type-independent chromatin signature of DNA hypomethylation during aging. Analysis of scedasticity showed that interindividual variability of DNA methylation increased during aging in MSCs and differentiated cells, providing a new avenue for the identification of DNA methylation changes over time. DNA methylation profiling of genetically identical individuals showed that both the tendency of DNA methylation changes and scedasticity depended on non-genetic as well as genetic factors. Our results indicate that the dynamics of DNA methylation during aging depend on a complex mixture of factors that include the DNA sequence, cell type and chromatin context involved, and that, depending on the locus, the changes can be modulated by genetic and/or external factors. Total DNA isolated by standard procedures from peripheral blood of 24 samples obtained from 12 pairs of MZ twins aged 21 to 66.
2014-09-25 | E-GEOD-52113 | biostudies-arrayexpress
Project description:In differentiated cells, aging is associated with hypermethylation of DNA regions enriched in repressive histone posttranslational modifications. However, the chromatin marks associated with changes in DNA methylation in adult stem cells during lifetime are still largely unknown. Here, DNA methylation profiling of mesenchymal stem cells obtained from individuals aged 2 to 92 identified 18735 hypermethylated and 45407 hypomethylated CpG sites associated with aging. As in differentiated cells, hypermethylated sequences were enriched in chromatin repressive marks. Most importantly, hypomethylated CpG sites were strongly enriched in the active chromatin mark H3K4me1 in stem and differentiated cells, suggesting this is a cell type-independent chromatin signature of DNA hypomethylation during aging. Analysis of scedasticity showed that interindividual variability of DNA methylation increased during aging in MSCs and differentiated cells, providing a new avenue for the identification of DNA methylation changes over time. DNA methylation profiling of genetically identical individuals showed that both the tendency of DNA methylation changes and scedasticity depended on non-genetic as well as genetic factors. Our results indicate that the dynamics of DNA methylation during aging depend on a complex mixture of factors that include the DNA sequence, cell type and chromatin context involved, and that, depending on the locus, the changes can be modulated by genetic and/or external factors. Total DNA isolated by standard procedures from human adult mesenchymal stem cells (MSCs) obtained from 34 individuals aged 2 to 92
2014-09-25 | E-GEOD-52112 | biostudies-arrayexpress