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Proteomic dataset of secretome derived from Placental mesenchymal stem cells

ABSTRACT: The use of perinatal MSCs remains largely unexplored. Consequently, there is a significant gap in knowledge regarding the optimal selection of perinatal MSCs and their appropriate administration to maximize the benefits for DFU treatment. Moreover, there is a lack of direct comparison among different types of perinatal MSCs. In this study, we aimed to address these gaps by comparing the secretome profiles of MSCs derived from human umbilical cord (UC), chorionic villi (CV), and decidua basalis (DC) of the human placenta. We utilized mass spectrometry to analyze the protein components in the secretome derived from hUCMSCs, hCVMSCs, and hDCMSCs. Over 1000 secreted proteins were quantified by mass spectroscopy in secretome of MSCs, with 435 being commonly expressed.

INSTRUMENT(S): Orbitrap Fusion Lumos

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

SUBMITTER: Xiaohua Jiang, School of Biomedical Sciences, Faculty of Medicine

PROVIDER: MSV000095571 | MassIVE | Sat Aug 10 05:26:00 BST 2024

SECONDARY ACCESSION(S): PXD054775

REPOSITORIES: MassIVE

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Project description:BACKGROUND: Ischemia/reperfusion injury (IRI) is the leading cause of acute kidney injury (AKI). The current standard of care focuses on supporting kidney function, stating the need for more efficient and targeted therapies to enhance repair. Mesenchymal Stromal Cells (MSCs) and their secretome, either as conditioned medium (CM) or extracellular vesicles (EVs), have emerged as promising options for regenerative therapy, however, their full potential in treating AKI remains unknown.METHODS: In this study, we employed an in vitro model of chemically-induced ischemia using antimycin A combined with 2-deoxy-D-glucose to induce ischemic injury in proximal tubule epithelial cells. Afterwards, we evaluated the effects of MSC secretome, CM or EVs obtained from adipose tissue, bone marrow and umbilical cord, on ameliorating the detrimental effects of ischemia. To assess the damage and treatment outcomes, we analyzed cell morphology, mitochondrial health parameters (mitochondrial activity, ATP production, mass and membrane potential) and overall cell metabolism by metabolomics.RESULTS: Our findings show that ischemic injury caused cytoskeletal changes confirmed by disruption of the F-actin network, energetic imbalance as revealed by a 50% decrease in the oxygen consumption rate, increased oxidative stress, mitochondrial dysfunction and reduced cell metabolism. Upon treatment with MSC secretome, the morphological derangements were partly restored and ATP production increased by 40-50%, with umbilical cord-derived EVs being most effective. Furthermore, MSC treatment led to phenotype restoration as indicated by an increase in cell bioenergetics, including increased levels of glycolysis intermediates, as well as an accumulation of antioxidant metabolites.CONCLUSION: Our in vitro model effectively replicated the in vivo-like morphological and molecular changes observed during ischemic injury. Additionally, treatment with MSC secretome ameliorated proximal tubule damage, highlighting its potential as a viable therapeutic option for targeting AKI.

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Proteomic dataset of secretome derived from Placental mesenchymal stem cells

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