The role of PPARgamma signaling in neuropathic pain development
| Project/Area Number |
23790649
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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 |
Pain science
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| Research Institution | Kagoshima University |
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Principal Investigator |
HASEGAWA MAIKO 鹿児島大学, 医学部・歯学部附属病院, 講師 (20516637)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
Fiscal Year 2013: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2012: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2011: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
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| Keywords | 慢性疼痛 / マクロファージ極性 / PPARgamma / 鎮痛 / マクロファージ / 疼痛 / 炎症性疼痛 |
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| Research Abstract |
Peroxisome proliferator-activated receptor (PPAR) gamma signaling is known to regulate heterogeneity of macrophages, which are often referred to as proinflammatory (M1) and anti-inflammatory (M2) macrophages. M1 macrophages have considerable antimicrobial activity whereas M2 macrophages are involved in wound healing process. We investigated the link between the phenotype switching of macrophage polarization induced by PPAR gamma signaling and pain development. Rosiglitazone significantly ameliorated mechanical allodynia by regulating macrophage infiltration at the inflamed site. The number of M1 macrophages was decreased whereas numbers of M2 macrophages were increased in rosiglitazone-treated sites. We speculate that rosiglitazone significantly alleviated the development of chronic pain, possibly through regulating macrophage polarity at the inflamed site. PPARgamma signaling in macrophages may be a potential therapeutic target for the treatment of pain development.
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Report
(4 results)
Research Products
(27 results)
