| Project/Area Number |
16K19657
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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 |
Pediatrics
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| Research Institution | Kagoshima University |
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Principal Investigator |
Ueno Kentaro 鹿児島大学, 医歯学域附属病院, 講師 (20644892)
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| Project Period (FY) |
2016-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2017: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2016: ¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
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| Keywords | 川崎病 / 冠動脈瘤 / 血管炎 / 小児科 / 細胞恒常性 / 細胞死 / 細胞の恒常性 / 免疫グロブリン / スタチン / ネクローシス / 細胞生存シグナル / 細胞障害 / 細胞生存 |
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| Outline of Final Research Achievements |
Prednisolone (PSL) is considered as preemptive primary treatment in combination with intravenous immunoglobulin (IVIG), especially for predicted IVIG non-responders. We focused on the pathogenesis of early KD vasculitis by examining the balance between endothelial cell survival and death, using serum activity from KD patients before IVIG to stimulate in vitro human coronary artery endothelial cells (HCAECs). We revealed that IG and a combination of IG and PSL treatments inhibited KD serum activated HCAECs proliferation and cytotoxicity mediated necrosis, decreased levels of HMGB-1, NF-κB p65 and IL-6, increased levels of soluble RAGE, and decreased Akt and ERK1/2 phosphorylation. Furthermore, we revealed that PSL treatment have potentiate inhibitory effect on HMGB-1 induced inflammatory response via a suppression of NF-κB p65 and ERK 1/2 activation. PSL treatment may be an effective to suppress HMGB-1-mediated inflammatory responses in acute phase of KD vasculitis.
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