| Project/Area Number |
21792079
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Orthodontic/Pediatric dentistry
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| Research Institution | The University of Tokushima |
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Principal Investigator |
KINOUCHI Nao The University of Tokushima, 病院, 助教 (30457329)
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| Project Period (FY) |
2009 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2010: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2009: ¥3,380,000 (Direct Cost: ¥2,600,000、Indirect Cost: ¥780,000)
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| Keywords | 歯科矯正学 / アテロコラーゲン / RNAi / マイオスタチン / 骨格筋 |
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| Research Abstract |
In this study, we examined whether systemic administration of the myostatin-siRNA /ATCOL (Mst-siRNA / ATCOL) complex effectively silenced myostatin expression in caveolin-3-deficient mouse model of limb-girdle muscular dystrophy 1C(LGMDIC) mice. We observed the enlargement of a number of skeletal muscles, and more in mice treated with Mst-siRNA /ATCOL muscles than control. Moreover, the average myofibril size for Mst-siRNA / ATCOL-treated muscle was increased by approximately 1. 2-fold relative to control. We evaluated the contractile properties of Mst-siRNA / ATCOL-treated LGMDIC muscle. Hypertrophied Mst-siRNA-positive LGMDIC fibers seemed to improve contractile force generation. Notably, the level of contractile force was improved by approximately 60% in Mst-siRNA / ATCOL-treated wild type muscles relative to control. These results provide evidence that ATCOL-mediated systemic administration of siRNAs may be a powerful therapeutic tool for muscular atrophy.
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