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From the Department of Medicine, Division of Rheumatology, Mayo Clinic and Foundation, Rochester, Minnesota
Inflammation of the arterial wall in giant cell arteritis induces a
series of structural changes, including the formation of new
vasa vasorum. To study the regulation of neoangiogenesis in giant cell
arteritis, temporal arteries were examined for the extent and
localization of microvessel generation and for the production of
angiogenic factors. In normal arteries, vasa vasorum were
restricted to the adventitia, but in inflamed arteries,
capillaries emerged in the media and the intima. These capillaries
displayed a distinct topography with a circumferential arrangement in
the external one-third of the intima. Neovascularization was closely
correlated with the formation of lumen-obstructing intima, the
fragmentation of the internal elastic lamina, and the presence
of multinucleated giant cells. Comparison of tissue cytokine
transcription in temporal arteries of giant cell arteritis patients
with and without up-regulated neoangiogenesis identified interferon-
and vascular endothelial growth factor but not fibroblast growth
factor-2 as mediators associated with vasa vasorum proliferation. Giant
cells and CD68-positive macrophages at the media-intima junction were
found to be the major cellular sources of vascular endothelial growth
factor. These data demonstrate that formation of new vasa vasorum in
vasculitis is regulated by inflammatory cells and not by arterial wall
cells, raising the possibility that it represents a primary
disease mechanism and not a secondary hypoxia-induced event. Increased
neovascularization in interferon--rich arteries suggests that the
formation of new vasa vasorum is determined by the nature of the immune
response in the arterial wall, possibly resulting from the
generation and functional activity of multinucleated giant
cells.
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