The regulation mechanisms of chronic pain via ER-stress pathway in fibromyalgia
Project/Area Number |
26461476
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Collagenous pathology/Allergology
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Research Institution | Tokyo Medical University |
Principal Investigator |
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Co-Investigator(Kenkyū-buntansha) |
中島 利博 東京医科大学, 医学部, 教授 (90260752)
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Project Period (FY) |
2014-04-01 – 2017-03-31
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Project Status |
Completed (Fiscal Year 2016)
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Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
|
Keywords | 線維筋痛症 / 疼痛 / 視床下部 / 小胞体ストレス / ミトコンドリア |
Outline of Final Research Achievements |
Fibromyalgia (FM) is a chronic pain syndrome with unknown etiology. Then the decisive treatments for FM have not been established. We focused on ER stress signals and function of mitochondria in FM. In this study, we attempted to establish the neuron specific synoviolin (SYVN1) deficient mice and an inflammation model mice in the central nerves system (CNS) with HPV vaccine as pathological animal models of FM. Then we analyzed the lesions and pathological mechanisms of FM using these mice and tissues derived from patients with FM. The SYVN1 deficient mice had the morphological abnormality in the CNS. The mouse vaccinated with HPV vaccine showed neurological phenotypes that include low responsiveness of the tail reflex and locomotive mobility. Pathological analyses of these mice revealed the damage to the hypothalamus. These data indicated that these model mice were useful for analyses of FM pathology and the hypothalamus could have important roles for symptoms of FM.
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Report
(4 results)
Research Products
(25 results)
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[Journal Article] The E3 ligase synoviolin controls body weight and mitochondrial biogenesis through negative regulation of PGC-1β.2015
Author(s)
Fujita H, Yagishita N, Aratani S, Saito-Fujita T, Morota S, Yamano Y, Hansson MJ, Inazu M, Kokuba H, Sudo K, Sato E, Kawahara K, Nakajima F, Hasegawa D, Higuchi I, Sato T, Araya N, Usui C, Nishioka K, Nakatani Y, Maruyama I, Usui M, Hara N, Uchino H, Elmer E, Nishioka K, Nakajima T.
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Journal Title
EMBO J.
Volume: 34
Issue: 8
Pages: 1042-55
DOI
Related Report
Peer Reviewed / Open Access
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