2006 Fiscal Year Final Research Report Summary
Development of new cardiovascular regeneration therapy by regulating apoptosis and bone marrow stem cell mobilization
| Project/Area Number |
16590667
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Circulatory organs internal medicine
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| Research Institution | Shinshu University |
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Principal Investigator |
TAKAHASHI Masafumi Shinshu University, Department of Organ Regeneration, Associate Professor, 大学院医学系研究科, 助教授 (40296108)
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| Co-Investigator(Kenkyū-buntansha) |
ISE Hirohiko Shinshu University, Department of Organ Regeneration, Assistant professor, 大学院医学系研究科, 助手 (10324253)
IKEDA Uichi Shinshu University, Department of Organ Regeneration, Professor, 大学院医学系研究科, 教授 (30221063)
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| Project Period (FY) |
2004 – 2006
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| Keywords | cytokine / atherosclerosis / myocardial infarction / myocarditis / regeneration / bone marrow / angiogenesis |
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| Research Abstract |
We have previously reported the effectiveness and safety of therapeutic angiogenesis by transplantation of autologous bone marrow cells to ischemic limbs ; however, this therapy needs general anesthesia to obtain bone marrow cells. To develop more efficient therapy using bone marrow cells, we examined the effect of several factors, such as G-CSF, M-CSF, and erythropoietin (EPO), that regulate apoptosis and bone marrow cell mobilization in rat and murine models of cardiovascular diseases. The major findings of this study are : (1) G-CSF mobilized endothelial progenitor cells, accelerated reendothelialization, and decreased neointimal formation after vascular injury ; (2) M-CSF induced neointimal formation in the early stages after vascular injury through activation of SDF-1/CXCR4 system ; (3) EPO attenuated inflammatory cell infiltration and cytokine expression, and it improved cardiac function and reduced cardiac inflammation in autoimmune myocarditis. These findings suggest the therapeutic potential of these factors in cardiovascular diseases.
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