Abstract
SummaryMesenchymal progenitor cells have great therapeutic potential, yet incomplete characterization of their cell-surface interface limits their clinical exploitation. We have employed subcellular fractionation with quantitative discovery proteomics to define the cell-surface interface proteome of human bone marrow mesenchymal stromal/stem cells (MSCs) and human umbilical cord perivascular cells (HUCPVCs). We compared cell-surface-enriched fractions from MSCs and HUCPVCs (three donors each) with adult mesenchymal fibroblasts using eight-channel isobaric-tagging mass spectrometry, yielding relative quantification on >6,000 proteins with high confidence. This approach identified 186 upregulated mesenchymal progenitor biomarkers. Validation of 10 of these markers, including ROR2, EPHA2, and PLXNA2, confirmed upregulated expression in mesenchymal progenitor populations and distinct roles in progenitor cell proliferation, migration, and differentiation. Our approach has delivered a cell-surface proteome repository that now enables improved selection and characterization of human mesenchymal progenitor populations.
Highlights
Mesenchymal progenitor cells have major therapeutic potential, exemplified by their beneficial effects in preclinical and phase I/II clinical trials after stroke and myocardial infarction (Honmou et al, 2012; Lee et al, 2009) and in ameliorating immune responses in graft-versus-host disease (Kim et al, 2013)
Characteristics of mesenchymal stromal/stem cells (MSCs), human umbilical cord perivascular cells (HUCPVCs), and HDFs First, we compared the expression of known MSC surface markers and multilineage potential of primary bone marrow MSC, HUCPVC, and HDF cultures, each from three donors
HDFs expressed similar levels of CD73, CD90, and CD166 compared with MSCs and HUCPVCs (Figure 1A), but they did not exhibit multipotency
Summary
Mesenchymal progenitor cells have major therapeutic potential, exemplified by their beneficial effects in preclinical and phase I/II clinical trials after stroke and myocardial infarction (Honmou et al, 2012; Lee et al, 2009) and in ameliorating immune responses in graft-versus-host disease (Kim et al, 2013). Differentiation of these cells along mesenchymal lineages is a major therapeutic feature (Pittenger et al, 1999). Deciphering their cell-surface proteomes is an essential step in enabling the rigorous selection of progenitor populations and understanding their biology, both essential for controlling cell fate and tissue repair
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