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(Journal of Leukocyte Biology. 2000;68:1-8.)
© 2000 by Society for Leukocyte Biology

CXC chemokines in angiogenesis

John A. Belperio{dagger}, Michael P. Keane{dagger}, Douglas A. Arenberg{dagger}, Christina L. Addison{dagger}, Jan E. Ehlert{dagger}, Marie D. Burdick* and Robert M. Strieter*

* Department of Medicine, Division of Pulmonary and Critical Care Medicine, University of California, Los Angeles School of Medicine; and
{dagger} Department of Internal Medicine, Division of Pulmonary and Critical Medicine, The University of Michigan Medical School, Ann Arbor

Correspondence: Robert M. Strieter, M.D., Division of Pulmonary and Critical Care Medicine, Department of Medicine, UCLA School of Medicine, Room 37-131B, CHS, Box 951690, 10833 Le Conte Ave., Los Angeles, CA 90095-1690. E-mail: rstrieter{at}mednet.ucla.edu

A variety of factors have been identified that regulate angiogenesis, including the CXC chemokine family. The CXC chemokines are a unique family of cytokines for their ability to behave in a disparate manner in the regulation of angiogenesis. CXC chemokines have four highly conserved cysteine amino acid residues, with the first two cysteine amino acid residues separated by one non-conserved amino acid residue (i.e., CXC). A second structural domain within this family determines their angiogenic potential. The NH2 terminus of the majority of the CXC chemokines contains three amino acid residues (Glu-Leu-Arg: the ELR motif), which precedes the first cysteine amino acid residue of the primary structure of these cytokines. Members that contain the ELR motif (ELR+) are potent promoters of angiogenesis. In contrast, members that are inducible by interferons and lack the ELR motif (ELR-) are potent inhibitors of angiogenesis. This difference in angiogenic activity may impact on the pathogenesis of a variety of disorders.

Key Words: cytokines • neovascularization • wound repair • tumorigenesis • tumor metastasis


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