| Project/Area Number |
23791631
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Orthopaedic surgery
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| Research Institution | University of Fukui |
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Principal Investigator |
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| Project Period (FY) |
2011 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2012: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2011: ¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
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| Keywords | 骨 / 脊椎脊髄病学 / 骨髄間質細胞 / 脊髄損傷 / 細胞移植 / 神経再生 / 急性脊髄損傷 |
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| Research Abstract |
The precise mechanisms through which transplanted MSC attenuate inflammation after SCI are still unclear. The transplanted MSC migrated within the injured spinal cord without differentiating into glial or neuronal elements. MSC transplantation was associated with marked changes in the SCI environment, with significant increases in IL-4 and IL-13 levels reductions in TNF-α and IL-6 levels. This was associated simultaneously with increased numbers of alternatively activated macrophages (M2 phenotype: arginase -1 or CD206-positive) and decreased numbers of classically activated macrophages (M1 phenotype: iNOS or CD16/32-positive). These changes were associated with functional locomotion recovery in the MSC transplanted group, which correlated with preserved axons, less scar tissue formation and increased myelin sparring. Our results suggested that acute transplantation of MSC after SCI modified the inflammatory environment by shifting the macrophage phenotype from M1 to M2, and that this may reduce the effects of the inhibitory scar tissue in the subacute/chronic phase after injury to provide a permissive environment for axonal extension and functional recovery.
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