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CD105 antagonizes the inhibitory signaling of transforming growth factor βl on human vascular endothelial cells
Author(s) -
LI CHENGGANG,
HAMPSON IAN N.,
HAMPSON LYNN,
KUMAR PAT,
BERNABEU CARMELO,
KUMAR SHANT
Publication year - 2000
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.14.1.55
Subject(s) - endoglin , angiogenesis , microbiology and biotechnology , vascular endothelial growth factor b , transforming growth factor , endothelial stem cell , transforming growth factor beta , vascular endothelial growth factor c , biology , vascular endothelial growth factor a , chemistry , cancer research , in vitro , vascular endothelial growth factor , stem cell , biochemistry , vegf receptors , cd34
CD105 (endoglin), a receptor for transforming growth factor β (TGFβ), is highly expressed in tissue‐cultured, activated endothelial cells in vitro and in tissues undergoing angiogenesis in vivo. The absence of CD105 in knockout mice leads to their death from defective vascular development, but the role of CD105 in the modulation of angiogenesis has not been elucidated. TGFβ1isa well‐recognized regulator of angiogenesis. Using an antisense approach, we have shown that inhibition of CD105 protein translation in cultured human endothelial cells enhances the ability of TGFβ1 to suppress growth and migration in these cells. The ability of endothelial cells to form capillary tubes was evaluated by the use of a 3‐dimensional collagen matrix system where TGFβ 1 not only reduced the length of capillary‐like structures, but also caused massive mortality in CD105‐deficient cells compared to control cultures. These results provide direct evidence that CD105 antagonizes the inhibitory effects of TGFβ1 on human vascular endothelial cells and that normal cellular levels of CD105 are required for the formation of new blood vessels.—Li, C., Hampson, I. N., Hampson, L., Kumar, P., Bernabeu, C., Kumar, S. CD105 antagonizes the inhibitory signaling of transforming growth factor b1 on human vascular endothelial cells. FASEB J . 14, 55–64(1999)