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Blood, 15 December 2000, Vol. 96, No. 13, pp. 4046-4054
CHEMOKINES
Functional expression of CCR1, CCR3, CCR4, and CXCR4
chemokine receptors on human platelets
Kenneth J. Clemetson,
Jeannine M. Clemetson,
Amanda
E. I. Proudfoot,
Christine A. Power,
Marco Baggiolini, and
Timothy N. C. Wells
From the Theodor Kocher Institute, University of Berne,
Berne, Switzerland; and Serono Pharmaceutical Research Institute SA,
Geneva, Switzerland.
Platelets are known to contain platelet factor 4 and
 -thromboglobulin,  -chemokines containing the CXC motif, but
recent studies extended the range to the -family characterized by
the CC motif, including RANTES and Gro-. There is also evidence for expression of chemokine receptors CCR4 and CXCR4 in platelets. This
study shows that platelets have functional CCR1, CCR3, CCR4, and CXCR4
chemokine receptors. Polymerase chain reaction detected chemokine
receptor messenger RNA in platelet RNA. CCR1, CCR3, and especially CCR4
gave strong signals; CXCR1 and CXCR4 were weakly positive. Flow
cytometry with specific antibodies showed the presence of a clear
signal for CXCR4 and weak signals for CCR1 and CCR3, whereas CXCR1,
CXCR2, CXCR3, and CCR5 were all negative. Immunoprecipitation and
Western blotting with polyclonal antibodies to cytoplasmic peptides
clearly showed the presence of CCR1 and CCR4 in platelets in amounts
comparable to monocytes and CCR4 transfected cells, respectively.
Chemokines specific for these receptors, including monocyte chemotactic
protein 1, macrophage inflammatory peptide 1, eotaxin, RANTES, TARC,
macrophage-derived chemokine, and stromal cell-derived factor 1, activate platelets to give Ca++ signals, aggregation, and
release of granule contents. Platelet aggregation was dependent
on release of adenosine diphosphate (ADP) and its interaction
with platelet ADP receptors. Part, but not all, of the
Ca++ signal was due to ADP release feeding back to its
receptors. Platelet activation also involved heparan or chondroitin
sulfate associated with the platelet surface and was inhibited by
cleavage of these glycosaminoglycans or by heparin or low molecular
weight heparin. These platelet receptors may be involved in
inflammatory or allergic responses or in platelet activation in human
immunodeficiency virus infection.
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