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Related Experiment Video

Updated: Apr 1, 2026

Investigating von Willebrand Factor Pathophysiology Using a Flow Chamber Model of von Willebrand Factor-platelet String Formation

Investigating von Willebrand Factor Pathophysiology Using a Flow Chamber Model of von Willebrand Factor-platelet String Formation

Published on: August 14, 2017

Platelet-derived VWF in the stroke spotlight.

Veronica H Flood¹

¹MEDICAL COLLEGE OF WISCONSIN.

|October 3, 2015

Summary

Platelet-derived von Willebrand factor (VWF) significantly contributes to ischemic stroke injury. Mice lacking platelet VWF showed normal bleeding and thrombosis, but normal VWF levels did not prevent stroke.

Area of Science:

Hematology
Neurology
Vascular Biology

Background:

Von Willebrand factor (VWF) is crucial for hemostasis and thrombosis.
VWF is synthesized by endothelial cells and stored in platelets.
The specific role of platelet-derived VWF in ischemic stroke is not fully understood.

Purpose of the Study:

To investigate the distinct roles of endothelial versus platelet-derived VWF in ischemic stroke.
To determine the contribution of platelet VWF to cerebral infarction.

Main Methods:

Generation of mouse models with specific VWF expression (endothelial only or platelet only).
Assessment of hemostasis using a tail bleeding model.
Evaluation of thrombosis using carotid artery ligation.

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Microfluidics in Assessing Platelet Function

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Last Updated: Apr 1, 2026

Investigating von Willebrand Factor Pathophysiology Using a Flow Chamber Model of von Willebrand Factor-platelet String Formation

Investigating von Willebrand Factor Pathophysiology Using a Flow Chamber Model of von Willebrand Factor-platelet String Formation

Published on: August 14, 2017

Microfluidics in Assessing Platelet Function

Microfluidics in Assessing Platelet Function

Published on: November 8, 2024

Live-cell Imaging of Platelet Degranulation and Secretion Under Flow

Live-cell Imaging of Platelet Degranulation and Secretion Under Flow

Published on: July 10, 2017

Induction of ischemic stroke via middle cerebral artery occlusion.

Main Results:

Mice lacking platelet-derived VWF but with endothelial VWF showed normal hemostasis and thrombosis.
Mice with only platelet-derived VWF exhibited defective hemostasis and thrombosis.
Mice with only platelet-derived VWF experienced significant cerebral infarction after middle cerebral artery occlusion.
VWF-deficient mice showed minimal infarcts, highlighting the role of VWF in stroke pathology.

Conclusions:

Platelet-derived VWF plays a critical and specific role in mediating ischemic stroke injury.
Endothelial VWF alone is insufficient to prevent stroke pathology in the absence of platelet VWF.
Targeting platelet VWF may offer a therapeutic strategy for ischemic stroke.