| Project/Area Number |
16590856
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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 |
Neurology
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| Research Institution | Kawasaki Medical School |
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Principal Investigator |
HAGIWARA Hiroki Kawasaki Medical School, Neurology, Assistant Professor, 医学部, 講師 (80276732)
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| Co-Investigator(Kenkyū-buntansha) |
MURAKAMI Tatsufumi Kawasaki Medical School, Neurology, Associate Professor, 医学部, 助教授 (30330591)
SUNADA Yoshihide Kawasaki Medical School, Neurology, Professor, 医学部, 教授 (00240713)
TESHIMA Takanori Kyushu University Hospital, Center for Cellular and Molecular Medicine, Associate Professor, 医学部, 助教授 (40284096)
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| Project Period (FY) |
2004 – 2005
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| Project Status |
Completed (Fiscal Year 2005)
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| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2005: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 2004: ¥2,200,000 (Direct Cost: ¥2,200,000)
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| Keywords | bone marrow transplantation / muscular dystrophy / regenerative medicine / EGFP mouse / dy mouse / mdx moude / extracellular matrix / laminin |
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| Research Abstract |
To evaluate the therapeutic potential of bone marrow, we examined whether pathogenesis in dystrophin-deficient (mdx) mice (a model for Duchenne muscular dystrophy [DMD]) and laminin alpha2-deficient (dy) mice (a model for congenital muscular dystrophy type 1A [MDC1A]) is ameliorated by bone marrow transplantation. We selected whole bone marrow cells for transplantation. Green fluorescent protein (GFP) mice were used as donors. Both model mice exhibited GFP-positive muscle fibers. In mdx mice, bone marrow transplantation failed to produce any significant differences in muscle pathology, although some GFP-positive fibers with restored dystrophin expression were observed. In contrast, in the dy mice, bone marrow transplantation led to a significant increase in lifespan and an increase in growth rate, muscle strength, and respiratory function. We conclude that bone marrow transplantation improved outcome in dy mice but not mdx mice. It is possible that bone marrow transplantation therapies designed to ameliorate muscular dystrophies are more likely to succeed in MDC1A than in DMD. Our results would open up the direct clinical application of bone marrow transplantation for muscular dystrophies such as MDC1A.
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