An article published this year in “PLOS ONE” using our CD105-PE (clone
2H6F11), by our customers from Unit of Blood Diseases and Stem Cells
Transplantation, Department of Clinical and Experimental Sciences, University
of Brescia, ASST Spedali Civili di Brescia, Italy, in the analysis of how
Mesenchymal stromal cells (MSCs) induce ex vivo proliferation and erythroid
commitment of cord blood haematopoietic stem cells (CB-CD34+ cells). Congrats
and Thanks.
Summary:
A human bone marrow-derived
mesenchymal stromal cell (MSCs) and cord blood-derived CD34+ stem cell
co-culture system was set up in order to evaluate the proliferative and
differentiative effects induced by MSCs on CD34+ stem cells, and the reciprocal
influences on gene expression profiles. After 10 days of co-culture,
non-adherent (SN-fraction) and adherent (AD-fraction) CD34+ stem cells were
collected and analysed separately. In the presence of MSCs, a significant
increase in CD34+ cell number was observed (fold increase = 14.68), mostly in
the SN-fraction (fold increase = 13.20). This was combined with a significant
increase in CD34+ cell differentiation towards the BFU-E colonies and with a
decrease in the CFU-GM. These observations were confirmed by microarray
analysis. Through gene set enrichment analysis (GSEA), we noted a significant
enrichment in genes involved in heme metabolism (e.g. LAMP2, CLCN3, BMP2K),
mitotic spindle formation and proliferation (e.g. PALLD, SOS1, CCNA1) and
TGF-beta signalling (e.g. ID1) and a down-modulation of genes participating in
myeloid and lymphoid differentiation (e.g. PCGF2) in the co-cultured CD34+ stem
cells. On the other hand, a significant enrichment in genes involved in
oxygen-level response (e.g. TNFAIP3, SLC2A3, KLF6) and angiogenesis (e.g.
VEGFA, IGF1, ID1) was found in the co-cultured MSCs. Taken together, our
results suggest that MSCs can exert a priming effect on CD34+ stem cells,
regulating their proliferation and erythroid differentiation. In turn, CD34+
stem cells seem to be able to polarise the BM-niche towards the vascular
compartment by modulating molecular pathways related to hypoxia and angiogenesis.
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