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Blood, 1 February 2005, Vol. 105, No. 3, pp. 1078-1084.
Prepublished online as a Blood First Edition Paper on September 30, 2004; DOI 10.1182/blood-2004-05-1827.


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Submitted May 13, 2004
Accepted September 20, 2004

von Willebrand factor accelerates platelet adhesion and thrombus formation on a collagen surface in platelet-reduced blood under flow conditions

Kazuhiko Tomokiyo*, Yuichi Kamikubo, Takako Hanada, Tatsuya Araki, Yasushi Nakatomi, Yoichi Ogata, Stephanie M Jung, Tomohiro Nakagaki, and Masaaki Moroi

Blood Products Research Department, The Chemo-Sero-Therapeutic Research Institute, Kaketsuken, Kumamoto, Japan
Blood Products Research Department, The Chemo-Sero-Therapeutic Research Institute, Kaketsuken, Kumamoto, Japan; Department of Cell Biology, Division of Vascular Biology, The Scripps Research Institute, La Jolla, CA, USA
Department of Protein Biochemistry, Institute of Life Science, Kurume University, Kurume, Japan

* Corresponding author; email: tomokiyo{at}kaketsuken.or.jp.

Plasma von Willebrand factor (VWF) has been identified as an indispensable factor for platelet adhesion and thrombus formation on a collagen surface under flow conditions. VWF binds to collagen and then tethers platelets to the collagen surface through interaction with platelet glycoprotein Ib and also contributes to the thrombus formation on the collagen surface. In the present study, we demonstrated that the addition of VWF/factor VIII (FVIII) complex or purified VWF (>2 ristocetin cofactor activity/mL) increased platelet adhesion to the collagen surface in platelet-reduced blood (~5 x 104 platelets/µL) to the normal level. VWF had no stimulatory effect when it was allowed to bind to the collagen surface before blood flow was initiated. Addition of an excess of FITC (fluorescein-5-isothiocyanate)-labeled VWF to platelet-reduced blood under these flow conditions demonstrated that the VWF was mainly incorporated into the platelet aggregates. These results indicated that the supplemented VWF stimulates the platelet adhesion onto the collagen surface by enhancing platelet aggregation in the platelet-reduced condition. This also suggests a possibility that supplementation of VWF to individuals with thrombocytopenia might be effective for increasing their hemostatic potential.


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