2002 Fiscal Year Final Research Report Summary
Differentiation of Mesenchymal Stem Cells in Bone Marrow
| Project/Area Number |
12557082
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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 | 展開研究 |
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| Research Field |
Hematology
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| Research Institution | Keio University (2002)
Kumamoto University (2000-2001) |
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Principal Investigator |
SUDA Toshio Keio University. School of Medicine, Professor, 医学部, 教授 (60118453)
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| Co-Investigator(Kenkyū-buntansha) |
HIRAO Atsushi Keio University, School of Medicine, Assistant Professor, 医学部, 助手 (90343350)
OHBO Kazuyuki Keio University, School of Medicine, Assistant Professor, 医学部, 助手 (70250751)
OIKE Yuichi Keio University, School of Medicine, Assistant Professor, 医学部, 講師 (90312321)
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| Project Period (FY) |
2000 – 2002
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| Keywords | osteoblast / osteoclast / RANK / ALCAM / mesenchymal stem cell / perichondrium / vascular invasion / ephrin-B2 |
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| Research Abstract |
We studied the linkage among osteogenesis, angiogenesis and hematopoiesis in bone marrow formation. Interaction between osteoclasts and osteoblasts is indispensable to form bone and bone cavity as hematopoietic tissues. RANK/RANKL provided new insights into the osteoclast differentiation pathway. We have established a pure osteoclast culture system by isolating precursor cells and cultured in the presence of M-CSF and soluble RANKL. This system revealed that differentiation of osteoclasts is anchorage-dependent and that osteoclastogenesis is completely inhibited by GM-CSF and switched to dendritic cell differentiation by suppression of c-Fos expression. On the other hand, we purified mesenchymal stem cells from perichondrial cells and characterized their differentiation. We show that chondrocytes inhibited the growth of vascular endothelial cells. Eph-ephrin signaling might be involved in the invasion of vascular cells. Now, we are trying to isolate osteoclast-specific molecules by DNA subtraction method between osteoclasts and macrophages derived from common precursor cells. Since these two types of cells express quite similar molecules, osteoclast-specific molecules are enriched. These osteoclast-specific molecules are targets to regulate the osteoclast function.
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