Journal
JOURNAL OF VASCULAR RESEARCH
Volume 41, Issue 6, Pages 491-498Publisher
KARGER
DOI: 10.1159/000081805
Keywords
vasculogenesis; angiogenesis; coronary tubulogenesis; quail heart explant model; embryo
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Background: Transforming growth factor-beta (TGF-beta) isoforms have been implicated as both pro- and anti-angiogenic modulators. In this study we addressed the roles of TGF-beta isoforms on coronary tubulogenesis. Methods: Embryonic (E6) quail ventricular specimens were explanted onto collagen gels allowing endothelial cells to migrate and form vascular tubes. Growth factors and/or neutralizing growth factor antibodies were added to the cultures. Endothelial cells were identified using a quail endothelial cell marker, QH1. Image analysis was used to quantify aggregate tube length. Results: Addition of any isoform (TGF-beta(1), TGF-beta(2) or TGF-beta(3)) virtually prevented tubulogenesis (>95% inhibition), while stimulation of tubulogenesis occurred by adding neutralizing antibodies to TGF-beta(3), but not to TGF-beta(1) or -beta(2). When all three isoforms were added, tubulogenesis was enhanced, indicating the key role of TGF-beta(3). Documentation of the inhibitory effect of TGF-beta isoforms on tubulogenesis is further supported by our experiments in which the marked enhancement of tube formation by bFGF and VEGF was negated when exogenous TGF-beta(1), - beta(2), or -beta(3) were added to the cultures. Conclusions: (1) TGF-beta(1), -beta(2) and - beta(3) each inhibits angiogenesis; ( 2) cooperation between the three TGF-beta isoforms and other angiogenic factors is essential for the regulation of normal tubulogenesis and (3) the stimulatory effect of VEGF or bFGF on tubulogenesis is negated by exogenous TGB-betas. Copyright (C) 2004 S. Karger AG, Basel.
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