| Project/Area Number |
17390270
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Endocrinology
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| Research Institution | Keio University (2006)
Kyoto University (2005) |
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Principal Investigator |
ITOH Hiroshi Keio University, School of Medicine, Professor, 医学部, 教授 (40252457)
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| Co-Investigator(Kenkyū-buntansha) |
YAMASHITA Jun Kyoto University, Institute of Frontier Science, Professor, 再生医科学研究所, 助教授 (50335288)
EBIHARA Ken Kyoto University, School of Medicine, Research Investigator, 医学研究科, 研究員 (70362514)
SUZUKI Satoshi Akita University, School of Medicine, Professor, 医学部, 教授 (10311565)
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| Project Period (FY) |
2005 – 2006
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| Project Status |
Completed (Fiscal Year 2006)
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| Budget Amount *help |
¥15,500,000 (Direct Cost: ¥15,500,000)
Fiscal Year 2006: ¥5,200,000 (Direct Cost: ¥5,200,000)
Fiscal Year 2005: ¥10,300,000 (Direct Cost: ¥10,300,000)
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| Keywords | ES cells / Metabolic syndome / Hormone / Endothelial cells / Vascular smooth muscle cells / Adipocytes / Regeneration medicine / Adrenomedullin / アドレメジュリン / Notch / VEGF / cAMP / 動脈 / 血管 |
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| Research Abstract |
This project was conducted to delineate the cell differentiation pathways involved in the pathogenesis of metabolic syndrome, that is, the differentiation pathway of mesenchymal cells ; vascular cells (endothelial cells and vascular smooth muscle cells), adipocytes and skeletal muscle cells, and examined the possibility of the re-differentiation therapy for metabolic syndrome, using human ES cells.
We established the culture methods to differentiate vascular cells, osteocytes/chondrocytes and adipocytes, using human ES cells and traced the cell surface marker expressions in these cells. Adrenomedullin (AM), the vasodilator hormones, was shown to augment endothelial differentiation of human ES cell-derived vascular progenitor cells (VPC). AM was further demonstrated to induce arterialization of ES cell-derived endothelial cells through Notch signaling pathway. We also reported that AM was expressed highly in adipocytes and co-culture of adipocytes and ES cell-derived VPC resulted in endothelial cell differentiation.
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