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| Status |
Public on Mar 19, 2020 |
| Title |
Differential DNA methylation encodes proliferation and senescence programs in human adipose-derived mesenchymal stem cells |
| Organism |
Homo sapiens |
| Experiment type |
Methylation profiling by high throughput sequencing
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| Summary |
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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| Overall design |
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.
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| Contributor(s) |
Pepin ME, Benincasa G, Infante T, Miceli M, Ceccarelli S, Megiorni F, Anastasiadou E, Della Valle G, Fatone G, Docimo L, Nicoletti GF, Marchese C, Wende AR, Napoli C |
| Citation missing |
Has this study been published? Please login to update or notify GEO. |
| NIH grant(s) |
| Grant ID |
Grant title |
Affiliation |
Name |
| F30 HL137240 |
GADD45B and Metabolic Memory in Diabetic Heart Failure |
UNIVERSITY OF ALABAMA AT BIRMINGHAM |
Mark Emile Pepin |
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| Submission date |
Oct 21, 2019 |
| Last update date |
Mar 20, 2020 |
| Contact name |
Mark Emile Pepin |
| E-mail(s) |
pepinme@gmail.com
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| Organization name |
University of Alabama at Birmingham
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| Department |
Biomedical Engineering
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| Lab |
Adam Wende Laboratory
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| Street address |
1825 University Blvd
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| City |
Birmingham |
| State/province |
AL |
| ZIP/Postal code |
35294-2182 |
| Country |
USA |
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| Platforms (1) |
| GPL16791 |
Illumina HiSeq 2500 (Homo sapiens) |
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| Samples (4)
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| Relations |
| BioProject |
PRJNA578673 |
| SRA |
SRP226451 |
| Supplementary file |
Size |
Download |
File type/resource |
| GSE139157_Table_S1_ASC_AZA.v.VEH_Annotated_DiffMeth.xlsx |
3.8 Mb |
(ftp)(http) |
XLSX |
SRA Run Selector |
| Raw data are available in SRA |
| Processed data are available on Series record |
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