Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

PRC2-AgeIndex: a universal biomarker of aging and rejuvenation [ChIP-seq]

ABSTRACT: DNA methylation (DNAm) is one of the most reliable biomarkers of aging across many mammalian tissues. While the age-dependent global loss of DNAm has been well characterized, age-dependent DNAm gain is less specified. Multiple studies have demonstrated that polycomb repressive complex 2 (PRC2) targets are enriched among the CpG sites which gain methylation with age. However, systematic whole-genome examination of all PRC2 targets in the context of aging methylome as well as determination of the pan-tissue or tissue-specific nature of these associations is lacking. Here, by analyzing DNAm data from different assays and from multiple young and old human and mouse tissues, we found that low-methylated regions (LMRs) which are highly bound by PRC2 in embryonic stem cells (PRC2 LMRs) gain methylation with age in all examined somatic mitotic cells. We also estimated that this epigenetic change represents around 90% of the age-dependent DNAm gain genome-wide. Therefore, we propose the “PRC2-AgeIndex,” defined as the average DNAm in PRC2 LMRs, as a universal biomarker of cellular aging in somatic cells. In addition, we demonstrate the application of this biomarker in the evaluation of different anti-aging interventions, including dietary restriction and partial epigenetic reprogramming.

ORGANISM(S): Homo sapiens

PROVIDER: GSE253773 | GEO | 2024/06/19

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

PRC2-AgeIndex: a universal biomarker of aging and rejuvenation [WGBS]

Project description:DNA methylation (DNAm) is one of the most reliable biomarkers of aging across many mammalian tissues. While the age-dependent global loss of DNAm has been well characterized, age-dependent DNAm gain is less specified. Multiple studies have demonstrated that polycomb repressive complex 2 (PRC2) targets are enriched among the CpG sites which gain methylation with age. However, systematic whole-genome examination of all PRC2 targets in the context of aging methylome as well as determination of the pan-tissue or tissue-specific nature of these associations is lacking. Here, by analyzing DNAm data from different assays and from multiple young and old human and mouse tissues, we found that low-methylated regions (LMRs) which are highly bound by PRC2 in embryonic stem cells (PRC2 LMRs) gain methylation with age in all examined somatic mitotic cells. We also estimated that this epigenetic change represents around 90% of the age-dependent DNAm gain genome-wide. Therefore, we propose the “PRC2-AgeIndex,” defined as the average DNAm in PRC2 LMRs, as a universal biomarker of cellular aging in somatic cells. In addition, we demonstrate the application of this biomarker in the evaluation of different anti-aging interventions, including dietary restriction and partial epigenetic reprogramming.

2024-06-19 | GSE253985 | GEO

Primary osteoporosis is not reflected by disease-specific DNA methylation or accelerated epigenetic age in blood

Project description:Osteoporosis is an age-related metabolic bone disease. Hence, osteoporotic patients might suffer from molecular features of accelerated aging, which is generally reflected by specific age-associated DNA methylation (DNAm) changes. In this study, we analyzed genome wide DNAm profiles of peripheral blood from patients with manifest primary osteoporosis and non-osteoporotic controls. Statistical analysis did not reveal any individual CG dinucleotides (CpG sites) with significant aberrant DNAm in osteoporosis. Subsequently, we analyzed if age-associated DNAm patterns are increased in OP. Using three independent age-predictors we did not find any evidence for accelerated epigenetic age in blood of osteoporotic patients. Taken together, osteoporosis is not reflected by characteristic DNAm patterns of peripheral blood that might be used as biomarker for the disease. The prevalence of osteoporosis is age-associated – but it is not associated with premature epigenetic aging in peripheral blood.

2018-03-13 | GSE99624 | GEO

DNA Methylation in PRDM8 is a Biomarker for Dyskeratosis Congenita

Project description:Dyskeratosis congenita (DKC) is characterized by impaired telomere maintenance and reveals clinical features of premature aging. So far, diagnosis of DKC relies particularly on telomere length screening raising the need for additional biomarkers. In this study, we analysed global DNA methylation (DNAm) profiles of DKC patients. Age-associated DNAm changes were not generally accelerated in DKC. However, we observed significant hypermethylation in the gene for PR domain containing 8 (PRDM8). Notably, the same genomic region revealed hypermethylation in aplastic anemia (AA), and Down syndrome (DS), indicating that there might be an association with premature aging syndromes. Site-specific analysis of DNAm level in PRDM8 with pyrosequencing and MassArray validated aberrant hypermethylation in 14 DKC patients and 27 AA patients. Notably, telomere length was not directly correlated with DNAm in PRDM8, indicating that the two methods are complementary. In conclusion, DNAm at PRDM8 provides a new biomarker to support diagnosis of of AA and DKC.

2016-05-23 | GSE75310 | GEO

Genome-wide DNA methylation in post-mortem hippocampus of patients with bipolar disorder and controls

Project description:Evidence suggests accelerated aging mechanisms in bipolar disorder (BD), including DNA methylation (DNAm) aging in blood. However, it is unknown whether such mechanisms are also evident in the brain. To investigate this, we interrogated genome-wide DNA methylation in postmortem hippocampus from 32 BD-I patients and 32 age-, sex-, and race-matched non-psychiatric controls from the NIMH Human Brain Collection Core.

2019-12-02 | GSE129428 | GEO

Transcription factor occupancy is linked to DNA methylation turnover at active regulatory regions [MeDIP-Seq]

Project description:Genome wide analysis revealed that distal regulatory elements form Low Methylated Regions (LMRs). Even though transcription factor binding is required for LMR formation, we show for the test case CTCF that actual occupancy does not distinguish DNA methylation states. However, in line with a dynamic model of binding and DNA methylation turnover, we find that the product of active demethylation, 5-hydroxymethylcytosine (5hmC), is enriched at LMRs. 5hmC is present at active regulatory regions in stem and somatic cells and as a result a substantial fraction of changes in 5hmC occurs at LMRs. This suggests that transcription factor binding mediates active turnover of DNA methylation as an integral part of reprogramming of regulatory regions. hMeDIP sequencing in mouse embryonic stem cells (ES) and derived neuronal progenitors (NP).

2013-12-24 | E-GEOD-39738 | biostudies-arrayexpress

Cell-free DNA Methylation Patterns in Aging and Their Association with Inflamm-aging

Project description:Background: Liquid biopsies analyzing cell-free DNA methylation in plasma offer a non-invasive diagnostic for diseases, with aging biomarker potential underexplored. Methods: Utilizing enzymatic methyl-seq (EM-seq), this study assessed cfDNA methylation patterns in aging with blood from 35 healthy individuals. Results: It found aging signatures, including higher cfDNA levels and variations in fragment sizes, plus over 2 million age-related differentially methylated CpG sites. A biological age predictive model based on 41 CpG sites showed a strong correlation with chronological age, verified by two datasets. Age-specific epigenetic shifts linked to inflammation were revealed through differentially methylated regions profiling and Olink proteomics. Conclusion: These findings indicate cfDNA methylation as a potential biomarker for aging, and it might exacerbate immunoinflammatory reactivity in older individuals.

2024-05-23 | GSE259312 | GEO

Transcription factor occupancy is linked to DNA methylation turnover at active regulatory regions [Bisulfite-Seq]

Project description:Genome wide analysis revealed that distal regulatory elements form Low Methylated Regions (LMRs). Even though transcription factor binding is required for LMR formation, we show for the test case CTCF that actual occupancy does not distinguish DNA methylation states. However, in line with a dynamic model of binding and DNA methylation turnover, we find that the product of active demethylation, 5-hydroxymethylcytosine (5hmC), is enriched at LMRs. 5hmC is present at active regulatory regions in stem and somatic cells and as a result a substantial fraction of changes in 5hmC occurs at LMRs. This suggests that transcription factor binding mediates active turnover of DNA methylation as an integral part of reprogramming of regulatory regions. CTCF ChIP bisulfite sequencing in mouse embryonic stem cells and whole genome shotgun bisulfite sequencing of RESTko mouse embryonic stem (ES) cells

2013-12-24 | E-GEOD-39736 | biostudies-arrayexpress

Transcription factor occupancy is linked to DNA methylation turnover at active regulatory regions [MeDIP-Seq]

2013-12-24 | GSE39738 | GEO

Transcription factor occupancy is linked to DNA methylation turnover at active regulatory regions [Bisulfite-Seq]

2013-12-24 | GSE39736 | GEO

A whole lifespan mouse multi-tissue DNA methylation clock

Project description:Age predictors based on DNA methylation levels at a small set of CpG sites, DNAm clocks, have been developed for humans and extended to several other species. Three currently available versions of mouse DNAm clocks were either created for individual tissues or tuned towards young ages. Here, we constructed a robust multi-tissue age predictor based on 435 CpG sites, which covers the entire mouse lifespan and remains unbiased with respect to any particular age group. It can successfully detect the effects of several lifespan-modulating interventions on biological age as well as the rejuvenation effect related to the transition from fibroblasts to iPSCs. We have carried out comparative analyses of available mouse DNAm clocks, which revealed their broad applicability, but also certain limitations to the use of tissue-specific and multi-tissue age predictors. Together, these tools should help address diverse questions in aging research.

2018-11-20 | GSE121141 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data