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dc.contributor.authorLi, Chenggang
dc.contributor.authorHampson, Ian N
dc.contributor.authorHampson, Lynne
dc.contributor.authorKumar, Patricia
dc.contributor.authorBernabeu, Carmelo
dc.contributor.authorKumar, Shant
dc.date.accessioned2009-11-23T11:34:36Z
dc.date.available2009-11-23T11:34:36Z
dc.date.issued2000-01
dc.identifier.citationCD105 antagonizes the inhibitory signaling of transforming growth factor beta1 on human vascular endothelial cells. 2000, 14 (1):55-64 FASEB J.en
dc.identifier.issn0892-6638
dc.identifier.pmid10627280
dc.identifier.urihttp://hdl.handle.net/10541/86681
dc.description.abstractCD105 (endoglin), a receptor for transforming growth factor beta (TGFbeta), 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. TGFbeta1 is a 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 TGFbeta1 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 TGFbeta1 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 TGFbeta1 on human vascular endothelial cells and that normal cellular levels of CD105 are required for the formation of new blood vessels.
dc.language.isoenen
dc.subject.meshAnimals
dc.subject.meshAntigens, CD
dc.subject.meshBase Sequence
dc.subject.meshCell Death
dc.subject.meshCell Movement
dc.subject.meshCells, Cultured
dc.subject.meshDNA Primers
dc.subject.meshEndothelium, Vascular
dc.subject.meshHumans
dc.subject.meshMice
dc.subject.meshNeovascularization, Physiologic
dc.subject.meshOligonucleotides, Antisense
dc.subject.meshRNA, Messenger
dc.subject.meshReceptors, Cell Surface
dc.subject.meshSignal Transduction
dc.subject.meshTransforming Growth Factor beta
dc.subject.meshVascular Cell Adhesion Molecule-1
dc.titleCD105 antagonizes the inhibitory signaling of transforming growth factor beta1 on human vascular endothelial cells.en
dc.typeArticleen
dc.contributor.departmentDepartment of Pathological Sciences, Medical School, University of Manchester, Manchester M13 9PT, U.K.en
dc.identifier.journalThe FASEB Journalen
html.description.abstractCD105 (endoglin), a receptor for transforming growth factor beta (TGFbeta), 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. TGFbeta1 is a 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 TGFbeta1 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 TGFbeta1 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 TGFbeta1 on human vascular endothelial cells and that normal cellular levels of CD105 are required for the formation of new blood vessels.


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