Please use this identifier to cite or link to this item: http://hdl.handle.net/11455/40318
標題: Syndecan-1 up-regulated by ephrinB2/EphB4 plays dual roles in inflammatory angiogenesis
作者: Yuan, K.
陳健尉
Hong, T.M.
Chen, J.J.W.
Tsai, W.H.
Lin, M.T.
關鍵字: heparan-sulfate proteoglycans;cell-surface proteoglycans;endothelial-cells;gene-expression;cardiovascular development;rheumatoid-arthritis;epithelial-cells;growth-factors;stromal cells;smooth-muscle
Project: Blood
期刊/報告no:: Blood, Volume 104, Issue 4, Page(s) 1025-1033.
摘要: 
EphrinB2 and EphB4, its cognate receptor, are important in the vascular development of the mouse embryo. Their roles in human inflammatory angiogenesis, however, are not well understood. By examining hyperinflammatory lesions, we saw that ephrinB2 was predominantly expressed in macrophage-like cells and EphB4 in small venules. Because macrophages usually transmigrate through postcapillary venules during inflammation, we wanted to explore the downstream effects of EphB4 after binding to ephrinB2. By using cDNA microarray technique and following reverse transcriptase-polymerase chain reaction (RT-PCR), we found that syntenin and syndecan-1 were up-regulated in EphB4-positive endothelial cells dose dependently and time dependently after stimulation with preclustered ephrinB2. In vitro, ephrinB2 suppressed the angiogenic effects of basic fibroblast growth factor (bFGF) on EphB4-positive endothelial cells, partially due to syndecan-l's competition with fibroblast growth factor receptor (FGFR) for bFGF. However, ephrinB2 exhibited angiogenic effects in vivo, possibly due to an inflammation-associated enzyme-heparanase. The enzymes could convert the inhibitory effect of ephrinB2 on EphB4-positive endothelial cells to an activating effect by removing poorly sulfated side chains of up-regulated syndecan-1 ectodomain. Depending on the presence of heparanases, the roles of syndecan-1 may be opposite in different physiological settings. (C) 2004 by The American Society of Hematology.
URI: http://hdl.handle.net/11455/40318
ISSN: 0006-4971
DOI: 10.1182/blood-2003-09-3334
Appears in Collections:生物醫學研究所

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