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Differential DNA methylation encodes proliferation and senescence programs in human adipose-derived mesenchymal stem cells

ABSTRACT: Differential DNA methylation encodes proliferation and senescence programs in human adipose-derived mesenchymal stem cells

PROVIDER: PRJNA578673 | ENA |

REPOSITORIES: ENA

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Differential DNA Methylation Encodes Proliferation and Senescence Programs in Human Adipose-Derived Mesenchymal Stem Cells.

Project description: Not available

| S-EPMC7174643 | biostudies-literature

Differential DNA methylation encodes proliferation and senescence programs in human adipose-derived mesenchymal stem cells

Project description:Adipose tissue-derived mesenchymal stem cells (ASC’s) constitute a vital population of multipotent cells capable of differentiating into end-organ tissues. However, scientific endeavors to harness the regenerative potential of ASC’s for regenerative medicine are currently limited by an incomplete understanding of the mechanisms that determine cell-lineage commitment and stemness. In the current study, we used reduced representation bisulfite sequencing (RRBS) analysis to identify epigenetic gene targets and cellular processes that are responsive to 5-azathioprine, a potent inducer of DNA methylation. In this manner, we describe specific changes to DNA methylation of ASCs to identify the critical pathways associated with ASC differentiation . We identified 4,797 differentially-methylated regions (FDR < 0.05) associated with 3,625 genes. Gene set enrichment analysis of the differentially-methylated target promoters identified phagocytosis, type 2 diabetes mellitus, and metabolic pathways as disproportionately hypomethylated, whereas adipocyte differentiation was the top most-enriched pathway to represent genes with hyper-methylated promoters. Interestingly, ZNF11 and ELK4 gene response elements were identified as genomic features most affected by DNA hypo- and hyper-methylation, respectively. Although further validation is needed, the implications of this pilot analysis provide the basis for understanding how epigenetic mechanisms influence the metabolic phenotype, and ultimately regenerative capacity, of ASC’s.

2020-03-19 | GSE139157 | GEO

Identification of heterogeneous senescence-associated transcriptional programs

Project description:Identification of heterogeneous senescence-associated transcriptional programs

| PRJEB19157 | ENA

Senescence-correlated gene expression programs of human prostate stromal cells in response to multiple proliferation-arresting stress and their potential in driving prostate neoplasia

Project description:As an age-related process, cellular senescence is cell cycle arrest and it safeguards against incidental oncogenic activation by playing antiproliferative roles. Despite the establishment that senescence is a beneficial anticancer mechanism, increasing evidence indicates its deleterious effects that might contribute to age-related pathologies. We applied a group of methods that causes typical senescence to PSC27, a primary normal human prostate stromal cell line, and compared their capacity in influencing the expression of senescence- and proliferation-related genes. Custom Agilent 44K whole human genome expression oligonucleotide microarrays were used to profile PSC27 prostate fibroblast cells treated with agents to induce senescence (oxidative stress, DNA damage, and radiation.) Total RNA was isolated and amplified prior to hybridization against a common reference pool of prostate tumor cell lines.

2012-07-22 | E-GEOD-26143 | biostudies-arrayexpress

Transcriptome-profiling (RNA-seq) and Ribosome-profiling (Ribo-seq) in proliferation, quiescence, senescence and transformed states.

Project description:We applied in parallel RNA-Seq and Ribosome-profiling analyses to immortalized human primary BJ fibroblast cells under the following conditions: normal proliferation, quiescence (induced by serum depletion), senescence (induced by activation of the oncogenic RASG12V gene, and examined at early (5 days; pre-senescent state) and late (14 days; fully senescent state) time points), and neoplastic transformation (induced by RASG12V in the background of stable p53 and p16INK4A knockdowns and SV40 small-T expression. RNA-seq, using Illumina HiSeq 2000, was applied to BJ cells under 5 conditions: proliferation, quiescence, pre-senescence, full-senescence, and transfomed. Ribosome profiling, using Illumina HiSeq 2000, was applied to BJ cells under 5 conditions: proliferation, quiescence, pre-senescence, full-senescence, and transfomed.

2013-03-24 | E-GEOD-42509 | biostudies-arrayexpress

Identification of heterogeneous senescence-associated transcriptional programs

Project description:We set out to characterize the transcriptional heterogeneity of the senescence program using a large number of whole-transcriptome sequencing datasets generated by us or publicly available. We identify a number of senescence transcriptional signatures associated to specific stresses or cell types. We also merge all the studies to identify and validate the genes that are universally differentially regulated during senescence.

2017-11-22 | E-MTAB-5403 | biostudies-arrayexpress

Senescence-correlated gene expression programs of human prostate stromal cells in response to multiple proliferation-arresting stress and their potential in driving prostate neoplasia

2012-07-23 | GSE26143 | GEO

Small Noncoding RNAome Changes during Human Bone Marrow Mesenchymal Stem Cells Senescence

Project description:The proliferation capability and functionality of BMSCs are known to decline with aging, which severely impairing the extensive applications of BMSCs-based therapies. In this study, replicative senescence model of hBMSCs was established and the expression changes of small noncoding RNAs during senescence was detected by small RNA high-throughput sequencing analysis and qPCR.

2021-12-27 | GSE192578 | GEO

Dynamic remodeling of translation programs drives hepatocyte proliferation during liver regeneration

Project description:Dynamic remodeling of translation programs drives hepatocyte proliferation during liver regeneration

| PRJNA415722 | ENA

Senescence-specific gene expression fingerprints

Project description:This SuperSeries is composed of the following subset Series: GSE3730: Replicative senescence in human fibroblasts GSE3731: Replicative senescence in post-selection HMECs Abstract: Replicative senescence is the state of irreversible proliferative arrest that occurs as a concomitant of progressive telomere shortening. By using cDNA microarrays and the gabriel system of computer programs to apply domain-specific and procedural knowledge for data analysis, we investigated global changes in gene transcription occurring during replicative senescence in human fibroblasts and mammary epithelial cells (HMECs). Here we report the identification of transcriptional "fingerprints" unique to senescence, the finding that gene expression perturbations during senescence differ greatly in fibroblasts and HMECs, and the discovery that despite the disparate nature of the chromosomal loci affected by senescence in fibroblasts and HMECs, the up-regulated loci in both types of cells show physical clustering. This clustering, which contrasts with the random distribution of genes down-regulated during senescence or up-regulated during reversible proliferative arrest (i.e., quiescence), supports the view that replicative senescence is associated with alteration of chromatin structure. Refer to individual Series

2006-03-06 | E-GEOD-4352 | biostudies-arrayexpress

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