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Blood, Vol. 95 No. 7 (April 1), 2000:
pp. 2304-2311
Eicosanoid regulation of angiogenesis: role of endothelial
arachidonate 12-lipoxygenase
Daotai Nie,
Keqin Tang,
Clement Diglio, and
Kenneth V. Honn
From the Departments of Radiation Oncology and Pathology, Wayne
State University School of Medicine, and the Karmanos Cancer Institute,
Detroit, MI.
Angiogenesis, the formation of new capillaries from preexisting
blood vessels, is a multistep, highly orchestrated process involving
vessel sprouting, endothelial cell migration, proliferation, tube
differentiation, and survival. Eicosanoids, arachidonic acid (AA)-derived metabolites, have potent biologic activities on vascular endothelial cells. Endothelial cells can synthesize various
eicosanoids, including the 12-lipoxygenase (LOX) product
12(S)-hydroxyeicosatetraenoic acid (HETE). Here we
demonstrate that endogenous 12-LOX is involved in endothelial cell
angiogenic responses. First, the 12-LOX inhibitor, N-benzyl-N-hydroxy-5-phenylpentanamide (BHPP), reduced endothelial cell
proliferation stimulated either by basic fibroblast growth factor
(bFGF) or by vascular endothelial growth factor (VEGF). Second,
12-LOX inhibitors blocked VEGF-induced endothelial cell migration, and this blockage could be partially reversed by the addition of 12(S)-HETE. Third, pretreatment of an angiogenic
endothelial cell line, RV-ECT, with BHPP significantly inhibited the
formation of tubelike/cordlike structures within Matrigel. Fourth,
overexpression of 12-LOX in the CD4 endothelial cell line significantly
stimulated cell migration and tube differentiation. In agreement with
the critical role of 12-LOX in endothelial cell angiogenic
responses in vitro, the 12-LOX inhibitor BHPP significantly
reduced bFGF-induced angiogenesis in vivo using a Matrigel implantation
bioassay. These findings demonstrate that AA metabolism in endothelial
cells, especially the 12-LOX pathway, plays a critical role in angiogenesis.
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