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Blood, 15 February 2001, Vol. 97, No. 4, pp. 937-945
HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY
Adenosine diphosphate strongly potentiates the ability of the
chemokines MDC, TARC, and
SDF-1 to stimulate platelet function
Adrian R. L. Gear,
Sudawadee Suttitanamongkol,
Delia Viisoreanu,
Renata K. Polanowska-Grabowska,
Sanghamitra Raha, and
David Camerini
From the Department of Biochemistry and Molecular
Genetics and the Department of Microbiology/Myles H. Thaler Center for
AIDS and Human Retrovirus Research, University of Virginia Health
Sciences Center; and the Department of Chemistry, University of
Virginia, Charlottesville, VA.
Platelet activation is normally induced by primary agonists
such as adenosine diphosphate (ADP), thrombin, and collagen, whereas other agonists, such as epinephrine, can play important accessory roles. It is now reported that the macrophage-derived chemokine (MDC),
thymus activation-regulated chemokine (TARC), and stromal cell-derived factor one (SDF-1) are highly effective activators of
platelet function under a variety of conditions, stimulating platelet
shape change, aggregation, and adhesion to collagen or fibrinogen.
Chemokine-mediated platelet activation was rapid and maximal (less than
5 seconds) under arterial flow conditions and depended strongly on the
presence of low levels of primary agonists such as ADP or thrombin.
Concentrations of ADP (0.05-0.25 µM) or thrombin (0.005-0.02 U/mL)
that induced minimal aggregation caused major aggregation acting in
combination with the chemokines. The ability of apyrase to block
chemokine-dependent aggregation or adhesion was consistent with an
important role for ADP. Chemokine-stimulated aggregation was also
insensitive to indomethacin, suggesting that the activation of
cyclo-oxygenase is not involved. TARC, MDC, and SDF-1 increased
intracellular calcium concentrations [Ca2+]i
when combined with low levels of ADP. The MDC and TARC receptor CCR4
was expressed on platelets, and an anti-CCR4 antibody blocked aggregation induced by TARC or MDC. Treatment of platelets with SDF-1
and MDC rapidly exposed P-selectin (CD62P) on the cell surface but did
not induce the secretion of serotonin. These findings suggest that the
chemokines MDC, TARC, and SDF-1, which may be produced during
inflammatory responses, coupled with low levels of ADP or thrombin, can
serve as strong stimuli for activating platelet function.
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