| Project/Area Number |
26861215
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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 | Tokai University |
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Principal Investigator |
IMAI Takeshi 東海大学, 医学部附属病院, 臨床助手 (60724672)
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| Project Period (FY) |
2014-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥3,380,000 (Direct Cost: ¥2,600,000、Indirect Cost: ¥780,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2014: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | 脊髄損傷 / 再髄鞘形成 / オリゴデンドロサイト前駆細胞 / アミロライド |
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| Outline of Final Research Achievements |
After spinal cord injury (SCI), secondary injury results in an expanding area of glial cell apoptosis. Oligodendrocyte precursor cells (OPCs) have been shown to actively proliferate within this expanding lesion, but a majority of these cells succumb to apoptosis instead of differentiating into functional oligodendrocytes. One of the factors that exacerbates secondary injury is endoplasmic reticulum (ER) stress. We previously reported that amiloride, an FDA-approved diuretic used to treat hypertension, enhances the ER stress response and suppresses apoptosis of glial cells in SCI rats. In this study, we labeled proliferating OPCs and demonstrated that amiloride treatment led to greater numbers of OPCs and also oligodendrocytes in the injured spinal cord. The increased MBP expression suggests that the increased numbers of mature oligodendrocytes led to improved remyelination, which significantly improved motor function recovery.
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