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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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			Action	DRS
	SRR10317242_1.fastq.gz	Fastqsanger.gz
	SRR10317242_2.fastq.gz	Fastqsanger.gz
	SRR10317243_1.fastq.gz	Fastqsanger.gz
	SRR10317243_2.fastq.gz	Fastqsanger.gz
	SRR10317244_1.fastq.gz	Fastqsanger.gz

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

Project description:Adult adipose tissue-derived mesenchymal stem cells (ASCs) constitute a vital population of multipotent cells capable of differentiating into numerous end-organ phenotypes. However, scientific and translational endeavors to harness the regenerative potential of ASCs 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'-azacitidine (5'-AZA). We describe specific changes to DNA methylation of ASCs, uncovering pathways likely associated with the enhancement of their proliferative capacity. We identified 4,797 differentially methylated regions (FDR < 0.05) associated with 3,625 genes, of which 1,584 DMRs annotated to the promoter region. Gene set enrichment of differentially methylated promoters identified "phagocytosis," "type 2 diabetes," and "metabolic pathways" as disproportionately hypomethylated, whereas "adipocyte differentiation" was the most-enriched pathway among hyper-methylated gene promoters. Weighted coexpression network analysis of DMRs identified clusters associated with cellular proliferation and other developmental programs. Furthermore, the ELK4 binding site was disproportionately hyper-methylated within the promoters of genes associated with AKT signaling. Overall, this study offers numerous preliminary insights into the epigenetic landscape that influences the regenerative capacity of human ASCs.

| 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.

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Project description:Identification of heterogeneous senescence-associated transcriptional programs

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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.

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METTL3-dependent m6A modification programs human neural progenitor cell proliferation

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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

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