Abstract
This study used in vivo molecular imaging to characterize endotheliall activation attributable to von Willebrand factor (vWF)-mediated platelet adhesion in atherosclerosis. In atherosclerotic mice lacking the low-density lipoprotein receptor on Western diet, the additional genetic deletion of the ADAMTS13, which cleaves endothelial-associated vWF, produced greater aortic molecular imaging signal for not only vWF and platelets, but also for endothelial adhesion molecules VCAM1 and P-selectin, larger plaque size, and lower aortic distensibility. Sustained ADAMTS13 therapy reduced signal for all 4 molecular targets and plaque size. We conclude that excess endothelial-associated vWF contributes to not only platelet adhesion, but also to up-regulation of endothelial cell adhesion molecules.
Original language | English (US) |
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Pages (from-to) | 1017-1028 |
Number of pages | 12 |
Journal | JACC: Basic to Translational Science |
Volume | 5 |
Issue number | 10 |
DOIs | |
State | Published - Oct 2020 |
Keywords
- atherosclerosis
- molecular imaging
- platelets
- von Willebrand factor
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine