Syndecan-1 up-regulated by ephrinB2/EphB4 plays dual roles in inflammatory angiogenesis

Kuo Yuan, Tse Ming Hong, Jeremy J.W. Chen, Wan Hua Tsai, Ming T. Lin

研究成果: Article

33 引文 (Scopus)

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-1'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.

原文English
頁(從 - 到)1025-1033
頁數9
期刊Blood
104
發行號4
DOIs
出版狀態Published - 2004 八月 15

指紋

Syndecan-1
Endothelial cells
Venules
Endothelial Cells
Macrophages
Fibroblast Growth Factor 2
Syntenins
Inflammation
Fibroblast Growth Factor Receptors
Polymerase chain reaction
RNA-Directed DNA Polymerase
Enzymes
Microarrays
Oligonucleotide Array Sequence Analysis
Reverse Transcriptase Polymerase Chain Reaction
Embryonic Development
Blood Vessels
Complementary DNA

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Immunology
  • Hematology
  • Cell Biology

引用此文

Yuan, Kuo ; Hong, Tse Ming ; Chen, Jeremy J.W. ; Tsai, Wan Hua ; Lin, Ming T. / Syndecan-1 up-regulated by ephrinB2/EphB4 plays dual roles in inflammatory angiogenesis. 於: Blood. 2004 ; 卷 104, 編號 4. 頁 1025-1033.
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abstract = "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-1'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.",
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Syndecan-1 up-regulated by ephrinB2/EphB4 plays dual roles in inflammatory angiogenesis. / Yuan, Kuo; Hong, Tse Ming; Chen, Jeremy J.W.; Tsai, Wan Hua; Lin, Ming T.

於: Blood, 卷 104, 編號 4, 15.08.2004, p. 1025-1033.

研究成果: Article

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