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Excessive Angiogenesis in von Willebrand Factor Knockout Mice is Accompanied by Increased Perivascular Coverage of Neovessels

L. Sommerville1, J. Xu1, D. Monroe2, M. Hoffman1,3

1Duke University, Durham, United States, 2University of North Carolina at Chapel Hill, Chapel Hill, United States, 3Veterans Affairs Medical Center, Durham, United States

Abstract Number: PB1526

Meeting: ISTH 2020 Congress

Theme: Platelet Disorders and von Willebrand Disease » von Willebrand Factor Biology

Background: Von Willebrand Factor (vWF) is an essential coagulation protein that is becoming recognized as a regulator of angiogenesis. Patients with acquired or congenital vWF deficiency exhibit dysregulated angiogenesis in the form of angiodysplastic lesions in the gut. The mechanisms that regulate angiodysplasia are unknown and current studies focus almost exclusively on the role of endothelial cells in vWF deficient angiogenesis.

Aims: Thus the goal of our study was to characterize the role of perivascular cells (pericytes) during angiogenesis in WT and vWF knockout (KO) mice using the aortic ring model.

Methods: Abdominal aortas were collected from mice aged 4 to 8 weeks, cut into 0.1 cm rings, and cultured for up to 21 days in collagen matrices. Neovessels sprouting from the rings were counted on selected days.

Results: On days 3, 7, and 10 vWF KO rings contained significantly more sprouts than WT
(p< 0.05, n= 30 rings). This difference resolved 14 days after embedding and the number of vessels remained similar until the experiment's end. At every time point WT and vWF KO vessels exhibited similar thickness, length, and number of branch points. In the aortic ring model the proliferative stage of angiogenesis peaks around day 7. Pericyte coverage and morphology were evaluated in 7-day-old cultures by immunofluorescent staining for the pericyte marker NG2. Images were captured by confocal microscopy and the area of NG2 staining was analyzed with Image J. vWF KO sprouts demonstrated significantly higher pericyte coverage than WT sprouts
(p< 0.05, n=52 images KO, n=43 images WT), with no discernible difference in pericyte morphology or localization along the vessels.

Conclusions: These data suggest that pericyte migration, adhesion and/or proliferation may be enhanced in the absence of vWF expression. This further suggests that pericytes play a role in the excessive angiogenesis that occurs in vWF KO conditions.

To cite this abstract in AMA style:

Sommerville L, Xu J, Monroe D, Hoffman M. Excessive Angiogenesis in von Willebrand Factor Knockout Mice is Accompanied by Increased Perivascular Coverage of Neovessels [abstract]. Res Pract Thromb Haemost. 2020; 4 (Suppl 1). https://abstracts.isth.org/abstract/excessive-angiogenesis-in-von-willebrand-factor-knockout-mice-is-accompanied-by-increased-perivascular-coverage-of-neovessels/. Accessed August 15, 2022.

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