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Blood, 1 February 2003, Vol. 101, No. 3, pp. 929-936
HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY
Dynamics of GPIIb/IIIa-mediated platelet-platelet interactions in
platelet adhesion/thrombus formation on collagen in vitro as revealed
by videomicroscopy
Dipti Patel,
Heikki Väänänen,
Markéta Jirou ková,
Thomas Hoffmann,
Carol Bodian, and
Barry S. Coller
From the Laboratory of Blood and Vascular Biology, The
Rockefeller University, New York, NY; and the Mount Sinai School of
Medicine, New York, NY.
The conventional description of platelet interactions with
collagen-coated surfaces in vitro, based on serial static measurements, is that platelets first adhere and spread to form a monolayer and then
recruit additional layers of platelets. To obtain dynamic information,
we studied gravity-driven platelet deposition in vitro on purified type
1 collagen by video phase-contrast microscopy at 22°C. With untreated
human and wild-type mouse platelets, soon after the initial adhesion of
a small number of "vanguard" platelets, "follower" platelets
attached to the spread-out vanguard platelets. Follower platelets then
adhered to and spread onto nearby collagen or over the vanguard
platelets. Thus, thrombi formed as a concerted process rather than as
sequential processes. Treatment of human platelets with monoclonal
antibody (mAb) 7E3 (anti-GPIIb/IIIa ( IIb 3) + V3) or tirofiban (anti-GPIIb/IIIa) did not prevent platelet
adhesion but nearly eliminated the deposition of follower platelets
onto vanguard platelets and platelet thrombi. Similar results were
obtained with Glanzmann thrombasthenia platelets. Wild-type
mouse platelets in the presence of mAb 1B5 (anti-GPIIb/IIIa) and
platelets from 3-null mice behaved like human platelets in the
presence of 7E3 or tirofiban. Deposition patterns of untreated human
and wild-type mouse platelets were consistent with random distributions
under a Poisson model, but those obtained with 7E3- and
tirofiban-treated human platelets, 1B5-treated mouse platelets, or
3-null platelets demonstrated a more uniform deposition than predicted. Thus, in this model system, absence or blockade of GPIIb/IIIa receptors interferes with thrombus formation and alters the
pattern of platelet deposition.
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