TITLE: PET imaging of brain macrophages using the peripheral benzodiazepine receptor in a macaque model of neuroAIDS

AUTHOR CONTACT:
Clayton A. Wiley
Presbyterian University Hospital, Pittsburgh, Pennsylvania, USA.
Phone: 412-647-0765
Fax: 412-647-5602
E-mail: wiley@np.awing.upmc.edu

View the PDF of this article at: https://www.the-jci.org/press/20227.pdf

VEGF-A Versatility

Lymphangiogenesis and hemangiogenesis are both important processes in angiogenesis, which plays a central role in tumor progression, chronic inflammatory disorders, and most blinding ocular diseases. The VEGF family of growth factors is a key contributor to these processes. Previous studies indicated that VEGF-A is primarily responsible for hemangiogenesis, whereas VEGF-C and -D induce lymphangiogenesis. Whether VEGF-A also plays a role in lymphangiogenesis, however, remains unclear. Wayne Streilein and colleagues, from The Schepens Eye Research Institute, addressed this concern by testing the effects of VEGF-A inhibition on both hemangiogenesis and lymphangiogenesis using a mouse model of suture-induced inflammatory corneal neovascularization (pages 10401050). By administration of a fusion protein that traps VEGF-A and specifically prevents activation of one of its receptors, VEGFR2, they showed that loss of VEGF-A function fully blocked both hemangiogenesis and lymphangiogenesis after suture placement. Furthermore, VEGF-A inhibition resulted in impaired recruitment of inflammatory cells into the cornea, and selective macrophage depletion in sutured corneas disabled corneal angiogenesis. These findings demonstrate critical roles for VEGF-A and for macrophages in the pathological induction of both
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Contact: Laurie Goodman
lgoodman@the-jci.org
212-342-4159
Journal of Clinical Investigation
2-Apr-2004