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Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, MI 48109;
Center for Vascular Biology and
Departments of Medicine and Cell Biology, Vanderbilt University Medical Center, Nashville, TN 37232;
§
Division of Pulmonary and Critical Care Medicine, Department of Medicine, University of California, Los Angeles School of Medicine, Los Angeles, CA 90095;
¶
Theodor Kocher Institute, Universitat Bern, Bern, Switzerland; and
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Department of Veteran’s Affairs, Vanderbilt University Medical Center, Nashville, TN 37232
We have previously shown that members of the ELR+ CXC
chemokine family, including IL-8; growth-related oncogenes 
, ß,
and 
; granulocyte chemotactic protein 2; and epithelial
neutrophil-activating protein-78, can mediate angiogenesis in the
absence of preceding inflammation. To date, the receptor on endothelial
cells responsible for chemotaxis and neovascularization mediated by
these ELR+ CXC chemokines has not been determined. Because
all ELR+ CXC chemokines bind to CXC chemokine receptor 2
(CXCR2), we hypothesized that CXCR2 is the putative receptor for
ELR+ CXC chemokine-mediated angiogenesis. To test this
postulate, we first determined whether cultured human microvascular
endothelial cells expressed CXCR2. CXCR2 was detected in human
microvascular endothelial cells at the protein level by both Western
blot analysis and immunohistochemistry using polyclonal Abs specific
for human CXCR2. To determine whether CXCR2 played a functional role in
angiogenesis, we determined whether this receptor was involved in
endothelial cell chemotaxis. We found that microvascular endothelial
cell chemotaxis in response to ELR+ CXC chemokines was
inhibited by anti-CXCR2 Abs. In addition, endothelial cell
chemotaxis in response to ELR+ CXC chemokines was sensitive
to pertussis toxin, suggesting a role for G protein-linked receptor
mechanisms in this biological response. The importance of CXCR2 in
mediating ELR+ CXC chemokine-induced angiogenesis in vivo
was also demonstrated by the lack of angiogenic activity induced by
ELR+ CXC chemokines in the presence of neutralizing Abs to
CXCR2 in the rat corneal micropocket assay, or in the corneas of
CXCR2-/- mice. We thus conclude that CXCR2 is the
receptor responsible for ELR+ CXC chemokine-mediated
angiogenesis.
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