| Project/Area Number |
25430122
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Tumor biology
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| Research Institution | Institute of Physical and Chemical Research |
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Principal Investigator |
Kitazume Shinobu 国立研究開発法人理化学研究所, 疾患糖鎖研究チーム, 副チームリーダー (80301753)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2015: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2014: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2013: ¥2,860,000 (Direct Cost: ¥2,200,000、Indirect Cost: ¥660,000)
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| Keywords | 血管内皮細胞 / 細胞接着 / PECAM / シアル酸 / レクチン / アポトーシス / 腫瘍血管新生 / ＰＥＣＡＭ / 腫瘍内血管新生 / α2,6-シアル酸 / 血管新生 / VEGF |
|---|
| Outline of Final Research Achievements |
We expected that platelet endothelial cell adhesion molecule (PECAM) would possess lectin-like activity toward α2,6-sialic acid to ensure its homophilic interaction. We found that a longer α2,6-sialylated oligosaccharide exhibited strong inhibitory activity against homophilic PECAM interaction in vitro. Furthermore, we found that a cluster-type α2,6-sialyl N-glycan probe specifically bound to PECAM-immobilized beads. Moreover, addition of the α2,6-sialylated oligosaccharide to endothelial cells enhanced the internalization of PECAM as well as the sensitivity to apoptotic stimuli. Collectively, these findings suggest that PECAM is a sialic acid-binding lectin and that this binding property supports endothelial cell survival. Notably, our findings that α2,6-sialylated glycans influenced the susceptibility to endothelial cell apoptosis shed light on the possibility of using a glycan-based method to modulate angiogenesis.
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