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Articles |
vß3 Integrin Expression in Normal and Atherosclerotic Artery
From the Department of Pathology, University of Washington, Seattle.
Correspondence to Masaaki Hoshiga, MD, PhD, University of Washington, Vascular Biology, Box 357335, Seattle, WA 98195.E-mail hoshiga@u.washington.edu.
Abstract Recent evidence suggests that
vß3 integrin is a critical molecule in
several processes involved in atherosclerosis
progression and in restenosis, eg, smooth muscle cell (SMC)
migration and angiogenesis. While several ligands for this integrin are
known to be present in atherosclerotic plaque, little is known
about the presence of
vß3 integrin at this
site. In the present study, we have examined
vß3 expression in normal and
atherosclerotic arteries. Thirty-six coronary artery
segments from the recipient hearts of 24 patients undergoing heart
transplantation were classified into two groups: nonatherosclerotic
diffuse intimal thickening (DIT) and atherosclerotic plaques. Serial
frozen sections were examined immunohistochemically with four different
monoclonal antibodies directed against human
vß3 complex or the ß3
subunit and with cell markers for SMCs, macrophages, and
endothelial cells. The endothelium
along the lumen of both DIT and plaque arteries showed high expression
of
vß3. The media of both DIT and plaque
arteries showed less intense but extensive expression of
vß3. Immunoprecipitation and
reverse-transcribed polymerase chain reaction (RT-PCR)
analyses performed on extracts from the aortic media confirmed
the presence of
vß3 in the media. In the
intima of both DIT and plaque arteries,
vß3 expression generally colocalized with
SMCs but rarely with macrophages. The microvessels in the
adventitia as well as in the plaque showed prominent expression of
vß3, in contrast to low expression
in similar-sized microvessels of the skin. These results suggest
that
vß3 is present both in the normal
artery and in sites of SMC accumulation and angiogenesis in
atherosclerotic plaques.
Key Words: immunohistochemistry
vß3 integrin atherosclerosis angiogenesis human
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