Molecular pathogenesis of neonatal fulminant dystrophic dog and fetal therapy
Project/Area Number |
21300157
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Research Category |
Grant-in-Aid for Scientific Research (B)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Laboratory animal science
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Research Institution | Shinshu University |
Principal Investigator |
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Co-Investigator(Kenkyū-buntansha) |
TAKEDA Shin'ichi 独立行政法人国立精神・神経医療研究センター, 神経研究所・遺伝子疾患治療研究部, 部長 (90171644)
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Project Period (FY) |
2009 – 2012
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Project Status |
Completed (Fiscal Year 2012)
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Budget Amount *help |
¥17,160,000 (Direct Cost: ¥13,200,000、Indirect Cost: ¥3,960,000)
Fiscal Year 2011: ¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2010: ¥5,720,000 (Direct Cost: ¥4,400,000、Indirect Cost: ¥1,320,000)
Fiscal Year 2009: ¥7,280,000 (Direct Cost: ¥5,600,000、Indirect Cost: ¥1,680,000)
|
Keywords | 疾患モデル / 筋ジストロフィー / 筋ジストロフィー犬 / ジストロフィン / 機械的ストレス / サイトカイン / ケモカイン / オステオポンチン / 即初期遺伝子 / ユートロフィン / ミオシン / マイクロアレイ / 前初期遺伝子 |
Research Abstract |
The dystrophic dog, a model of Duchene muscular dystrophy , shows a high mortality rate with a marked increase in serum creatine kinase (CK) levels in the neonatal period. By measuring serum CK levels in cord and venous blood, we found initial respiration resulted in massive diaphragm damage and lead to the high serum CK levels. cDNA microarray revealed that osteopontin was prominently upregulated even prior to the initial respiration and c-fos, egr-1, IL-6, and IL-8 were distinctly overexpressed after the respiration. These molecules could be associated with muscle damage in dystrophic muscle.
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Report
(4 results)
Research Products
(36 results)
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[Presentation] Multiple-exon skipping using cell-penetrating morpholinos for dystrophic dogs.2010
Author(s)
Yokota T, Saito T, Urasawa N, Nagata T, Nakamura A, Kore R, Sazani P, Partidge T, Takeda S, Hoffman E
Organizer
American society of gene & cell therapy 13thAnnual meeting
Place of Presentation
Washington DC, USA
Year and Date
2010-05-21
Related Report
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