Epigenetic regulation underlying development of chronic pain caused by adipokines
Project/Area Number |
21791469
|
Research Category |
Grant-in-Aid for Young Scientists (B)
|
Allocation Type | Single-year Grants |
Research Field |
Anesthesiology/Resuscitation studies
|
Research Institution | Wakayama Medical University |
Principal Investigator |
|
Project Period (FY) |
2009 – 2011
|
Project Status |
Completed (Fiscal Year 2011)
|
Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2011: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2010: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2009: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
|
Keywords | アディポサイトカイン / エピジェネティクス / ケモカイン / レプチン / マクロファージ / サイトカイン / MIP / ヒストン / 神経障害性疼痛 / 好中球 / CXCL2 / CCL3 |
Research Abstract |
Leptin, an adipokine, up-regulated the chemokine macrophage inflammatory proteins(MIPs) in macrophages. The expression of MIPs was increased in the injured peripheral nerves, and the blockade of MIPs signaling prevented nerve injury-induced neuropathic pain and neuroinflammation. Moreover, MIPs expression was enhanced by the overacetylation of histones. In conclusion, adipokines play key roles in the development of neuropathic pain, accompanied by epigenetic augmentation of chemokine expressions in inflammatory cells.
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Report
(4 results)
Research Products
(60 results)