Journal
GROWTH FACTORS
Volume 25, Issue 1, Pages 25-32Publisher
TAYLOR & FRANCIS LTD
DOI: 10.1080/08977190701272933
Keywords
RatB1a fibroblast; matrigel; angiogenesis; endothelial cell
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Funding
- NCI NIH HHS [CA87690, CA45518] Funding Source: Medline
- NHLBI NIH HHS [R01 HL076411] Funding Source: Medline
- NATIONAL CANCER INSTITUTE [R21CA087690] Funding Source: NIH RePORTER
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL076411] Funding Source: NIH RePORTER
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Blood vessel growth is critical for embryonic development and contributes to pathologies including cancer and diabetic retinopathy. A growing body of evidence suggests that signaling via the Wnt/beta-catenin pathway contributes to angiogenesis, and that paracrine Wnt signaling might alter endothelial cell function. To test the hypothesis that Wnt signaling promotes endothelial cell proliferation and vessel growth, we treated bovine aortic endothelial cells with Wnt1, Wnt2 and Wnt5a derived from coculture with Wnt-expressing fibroblasts. Endothelial cells cultured in the presence of Wnt1 displayed increased Wnt/beta-catenin signaling, proliferation and capillary stability in vitro. Wnt5a, which primarily signals via an alternate Wnt pathway, the Wnt/Ca++ pathway, decreased both cell number and capillary length. Wnt2, which in other cell types activates the Wnt/beta-catenin pathway, did not activate signaling, affect cell number or increase capillary length. These results suggest that Wnt/beta-catenin and Wnt/Ca++ signals might have opposing effects on angiogenesis.
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