| Project/Area Number |
16H05281
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
General internal medicine(including psychosomatic medicine)
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| Research Institution | Department of Clinical Research, National Hospital Organization Tokushima National Hospital |
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Principal Investigator |
KUROTA YUKIKO 独立行政法人国立病院機構徳島病院(臨床研究部), その他部局等, 研究員(移行) (70398014)
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| Co-Investigator(Kenkyū-buntansha) |
三ツ井 貴夫 独立行政法人国立病院機構徳島病院(臨床研究部), その他部局等, その他 (80294726)
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| Research Collaborator |
Kaji Ryuji
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| Project Period (FY) |
2016-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥17,420,000 (Direct Cost: ¥13,400,000、Indirect Cost: ¥4,020,000)
Fiscal Year 2018: ¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2017: ¥5,460,000 (Direct Cost: ¥4,200,000、Indirect Cost: ¥1,260,000)
Fiscal Year 2016: ¥7,930,000 (Direct Cost: ¥6,100,000、Indirect Cost: ¥1,830,000)
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| Keywords | パーキンソン病 / miRNA / パーキン / PARK2 / micro RNA / パーキンソン / microRNA |
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| Outline of Final Research Achievements |
In recent years, causative genes for familial Parkinson's disease have been discovered one after another, and it has been attempted to elucidate the pathogenesis of sporadic Parkinson's disease through its analysis. Parkin is the most frequent cause gene for familial Parkinson's disease (PARK2). We have identified several types of microRNAs bound to parkin in the intracellular mitochondrial and nuclear fractions as we proceeded to elucidate the pathogenesis of PARK2. Among them, it was suggested that parkin is involved in the processing of miR-132. Furthermore, the expression of miR-132 and pre-miR-132 in all fibroblasts (4 patients) obtained by skin biopsy of PARK2 patients showed a clear decrease compared to healthy controls.
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| Academic Significance and Societal Importance of the Research Achievements |
PARK2患者（4名）の皮膚生検により得た線維芽細胞において、その発現を健常対照と比較した。その結果、４患者すべてでmiR-132、pre-miR-132の発現は健常対照に比較して明らかな低下が認められた。この結果パーキンがmiR-132のprocessing/generationを促進していること、さらにmiR-132の発現抑制がPARK2 の病態の進展に関与していることを強く示唆するものであった。
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