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Blood, 15 November 2001, Vol. 98, No. 10, pp. 3143-3149
TRANSPLANTATION
Platelet-derived microparticles bind to hematopoietic
stem/progenitor cells and enhance their engraftment
Anna Janowska-Wieczorek,
Marcin Majka,
Jacek Kijowski,
Monika Baj-Krzyworzeka,
Ryan Reca,
A. Robert Turner,
Janina Ratajczak,
Steven G. Emerson,
M. Anna Kowalska, and
Mariusz Z. Ratajczak
From the Department of Pathology and Laboratory
Medicine, University of Pennsylvania School of Medicine, Philadelphia;
Department of Medicine, University of Alberta and Canadian Blood
Services, Edmonton, Alberta, Canada; Department of Transplantology
CMUJ, Krakow, Poland; and James Graham Brown Cancer Center, University
of Louisville, KY.
Because human CD34+ and murine Sca-1+
hematopoietic stem-progenitor cells (HSPCs) express platelet-binding
sialomucin P-selectin (CD162) and integrin Mac-1 (CD11b-CD18) antigen,
it was inferred that these cells might interact with platelets. As a
result of this interaction, microparticles derived from platelets
(PMPs) may transfer many platelet antigens (CD41, CD61, CD62, CXCR4, PAR-1) to the surfaces of HSPCs. To determine the biologic significance of the presence of PMPs on human CD34+ and murine
Sca-1+ cells, their expressions on mobilized peripheral
blood (mPB) and on nonmobilized PB- and bone marrow (BM)-derived
CD34+ cells were compared. In addition, the effects of PMPs
on the proliferation of CD34+ and Sca-1+ cells
and on adhesion of HSPCs to endothelium and immobilized SDF-1 were
studied. Finally, the hematopoietic reconstitution of lethally
irradiated mice receiving transplanted BM mononuclear cells
covered or not covered with PMPs was examined. It was found that PMPs are more numerous on mPB than on BM CD34+
cells, do not affect the clonogenicity of human and murine HSPCs, and
increase adhesion of these cells to endothelium and immobilized SDF-1.
Moreover, murine BM cells covered with PMPs engrafted lethally irradiated mice significantly faster than those not covered, indicating that PMPs play an important role in the homing of HSPCs. This could
explain why in a clinical setting human mPB HSPCs (densely covered with
PMPs) engraft more rapidly than BM HSPCs (covered with fewer
PMPs). These findings indicate a new role for PMPs in stem cell
transplantation and may have clinical implications for the optimization
of transplantations.

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