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Evaluation Of Wharton's Jelly Mesenchymal Stem Cells Secretome Profiling Derived In Time And Passage Dependent Manner

ABSTRACT: The data provided is from LCMS run of Wharton's Jelly Mesenchymal Stem Cells (WJMSC) derived secretomes. The samples consist of secretomes harvested at different time points (24, 48, and 72 hours) and passage numbers (P3, P5, and P10). The samples used were taken from 3 donors, with 3 technical runs for each sample. Thus, a total of 81 samples of data were collected. The research aims to understand how the composition of the secretome changes over time and with different cell passages. Advanced proteomic techniques are used to analyze the bioactive molecules secreted by WJMSCs, highlighting the impact of time and cell passage number on the therapeutic potential of these cells. This research seeks to enhance the clinical efficiency of WJMSCs for regenerative medicine applications by revealing the dynamic nature of their secretome.

INSTRUMENT(S): Orbitrap Fusion

ORGANISM(S): Homo Sapiens (ncbitaxon:9606)

SUBMITTER: Wan Safwani Wan Kamarul Zaman

PROVIDER: MSV000096363 | MassIVE | Sat Nov 09 00:44:00 GMT 2024

SECONDARY ACCESSION(S): PXD057695

REPOSITORIES: MassIVE

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Project description:Background: Human bone marrow mesenchymal stem cells (MSCs) expanded in vitro exhibit not only a tendency to lose their proliferative potential, homing ability and telomere length but also genetic or epigenetic modifications such as DNA methylation and the noncoding RNA-mediated mechanism. This results in the senescence of MSCs. We compared differential methylation patterns of genes and miRNAs between early-passage and late-passage cells and estimated the relationship between senescence and DNA methylation patterns. Genomic DNA of MSCs cultured at passage 5 (P5) and passage 15 (P15) was enriched using methylated DNA immunoprecipitation assays, and DNA methylation changes due to long-term culture of MSCs were analyzed using Human 2.1M Deluxe Promoter Arrays (NimbleGen). Results: When we analyzed the methylation differences between P5 and P15 more than twice, 3,338 genes showed more than two-fold higher methylation at P5 than P15, whereas 4,670 genes showed more than two-fold higher methylation at P15 than P5. When we examined hypermethylated genes (methylation peak ≥ 2) at P5 or P15, 2,739 genes, including those related to fructose and mannose metabolism and calcium signaling pathways, and 2,587 genes, including those related to DNA replication, cell cycle and the PPAR signaling pathway, were hypermethylated at P5 and P15, respectively. There was common hypermethylation of 1,205 genes at both P5 and P15. In addition, genes that were hypermethylated at P5 (CPEB1, GMPPA, CDKN1A, TBX2, SMAD9 and MCM2) showed lower mRNA expression than did those hypermethylated at P15, whereas genes that were hypermethylated at P15 (MAML2, FEN1 and CDK4) showed lower mRNA expression than did those that were hypermethylated at P5, demonstrating that hypermethylation at DNA promoter regions inhibited gene expression and that hypomethylation increased gene expression. In the case of hypermethylation on miRNA, 27 miRNAs were hypermethylated at P5, whereas 44 miRNAs were hypermethylated at P15. Conclusion: These results show that hypermethylation increases at genes related to DNA replication, cell cycle and adipogenic differentiation due to long-term culture, which may in part affect MSC senescence.

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Evaluation Of Wharton's Jelly Mesenchymal Stem Cells Secretome Profiling Derived In Time And Passage Dependent Manner

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