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A more recent version of this article appeared on December 1, 2006
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Submitted on April 20, 2006
Revised on September 18, 2006
Accepted on September 29, 2006
¶ ¶
*OB/GYN, Genetics and Development, Pathology, and ¶Institute of Cancer Genetics, Columbia University Medical Center, New York, NY 10032; Department of Cell and Developmental Biology, Weill Medical College of Cornell University, New York, NY 10021; ||Strang Cancer Research Laboratory at The Rockefeller University, New York, NY 10021
Monitoring Editor: Mark Ginsberg
Wnts are lipid-modified secreted glycoproteins that regulate diverse biological processes. We report that Wnt5a, which functions in noncanonical Wnt signaling, has activity on endothelial cells. Wnt5a is endogenously expressed in human primary endothelial cells and is expressed in murine vasculature at several sites in mouse embryos and tissues. Expression of exogenous Wnt5a in human endothelial cells promoted angiogenesis. Wnt5a induced noncanonical Wnt signaling in endothelial cells, as measured by Dishevelled and ERK1/2 phosphorylation, and inhibition of canonical Wnt signaling, a known property of Wnt5a. Wnt5a induced endothelial cell proliferation and enhanced cell survival under serum-deprived conditions. The Wnt5a-mediated proliferation was blocked by Frizzled-4 extracellular domain. Wnt5a expression enhanced capillary-like network formation, while reduction of Wnt5a expression decreased network formation. Reduced Wnt5a expression inhibited endothelial cell migration. Screening for Wnt5a-regulated genes in cultured endothelial cells identified several encoding angiogenic regulators, including matrix metalloproteinase-1, an interstitial collagenase, and Tie-2, a receptor for angiopoietins. Thus, Wnt5a acts through noncanonical Wnt signaling to promote angiogenesis.
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