The glycan engineering for mesenchymal stem cell migration
Project/Area Number |
24790105
|
Research Category |
Grant-in-Aid for Young Scientists (B)
|
Allocation Type | Multi-year Fund |
Research Field |
Biological pharmacy
|
Research Institution | National Institute of Health Sciences |
Principal Investigator |
SHINOBU Sakai 国立医薬品食品衛生研究所, 生化学部, 主任研究官 (60370938)
|
Research Collaborator |
ロバート サックステイン 米国ハーバード大学, 医学部, 教授
|
Project Period (FY) |
2012-04-01 – 2015-03-31
|
Project Status |
Completed (Fiscal Year 2014)
|
Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2014: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2013: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2012: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
|
Keywords | 間葉系幹細胞 / 糖鎖修飾 / 糖鎖リガンド / ホーミング / 再生医療 |
Outline of Final Research Achievements |
We analyzed whether enforced E-selectin ligand expression on murine mesenchymal stem cells (MSCs) could impact their effect in reversing autoimmune disease model mice. Although murine MSCs natively do not express the E-selectin-binding determinant sialyl Lewis x (sLex), we found that fucosyltransferase-mediated alpha (1,3)-exofucosylation of murine MSCs resulted in sLex display uniquely on cell surface CD44 thereby creating hematopoietic cell E-/L-selectin ligand (HCELL), the E-selectin-binding glycoform of CD44. The findings provide evidence that glycan engineering to enforce HCELL expression boosts trafficking of infused MSCs to inflamed site and substantially improves their efficacy in reversing autoimmune disease.
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Report
(4 results)
Research Products
(3 results)