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Blood, 15 June 2002, Vol. 99, No. 12, pp. 4486-4493
HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY
Endothelial von Willebrand factor recruits platelets to
atherosclerosis-prone sites in response to hypercholesterolemia
Gregor Theilmeier,
Carine Michiels,
Erik Spaepen,
Ingrid Vreys,
Désiré Collen,
Jos Vermylen, and
Marc F. Hoylaerts
From the Center for Molecular and Vascular Biology,
University of Leuven, Leuven, Belgium; Klinik und Poliklinik für
Anästhesiologie und operative Intensivmedizin, University of
Münster, Münster, Germany; and Laboratoire de Biochemie et
de Biologie Cellulaire, FUNDP, Namur, Belgium.
Platelets are thought to play a causal role during
atherogenesis. Platelet-endothelial interactions in vivo and
their molecular mechanisms under shear are, however, incompletely
characterized. Here, an in vivo platelet homing assay was used in
hypercholesterolemic rabbits to track platelet adhesion to plaque
predilection sites. The role of platelet versus aortic endothelial cell
(EC) activation was studied in an ex vivo flow chamber. Pathways of
human platelet immobilization were detailed during in vitro perfusion
studies. In rabbits, a 0.125% cholesterol diet induced no lesions
within 3 months, but fatty streaks were found after 12 months.
ECs at segmental arteries of 3- month rabbits expressed more von
Willebrand factor (VWF) and recruited 5-fold more platelets than
controls (P < .05, n = 5 and 4, respectively). The
3-month ostia had an increased likelihood to recruit platelets compared
to control ostia (56% versus 18%, P < .0001, n = 89
and 63, respectively). Ex vivo, the adhesion of 3-month platelets to
3-month aortas was 8.4-fold increased compared to control studies
(P < .01, n = 7 and 5, respectively). In
vitro, endothelial VWF-platelet glycoprotein (GP) Ib
and platelet P-selectin- endothelial P-selectin glycoprotein ligand 1 interactions accounted in combination for 83% of
translocation and 90% of adhesion (P < .01, n = 4) of
activated human platelets to activated human ECs. Platelet tethering
was mainly mediated by platelet GPIb , whereas platelet GPIIb/IIIa
contributed 20% to arrest (P < .05). In conclusion,
hypercholesterolemia primes platelets for recruitment via VWF, GPIb,
and P-selectin to lesion-prone sites, before lesions are detectable.
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