2013 Fiscal Year Final Research Report
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 |
Research Field |
Pain science
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Research Institution | Kagoshima University |
Principal Investigator |
HASEGAWA MAIKO 鹿児島大学, 医学部・歯学部附属病院, 講師 (20516637)
|
Project Period (FY) |
2011 – 2013
|
Keywords | 慢性疼痛 / マクロファージ極性 / PPARgamma |
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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