A new therapeutic strategy by suppression of F-actin/DNGR-1 signal in a rat model of crush injury

• Project/Area Number: 26861521
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Emergency medicine
• Research Institution: Osaka University
• Principal Investigator: Matsumoto Hisatake 大阪大学, 医学部附属病院, 医員 (70644003)
• Project Period (FY): 2014-04-01 – 2016-03-31
• Project Status: Completed (Fiscal Year 2015)
• Budget Amount: ¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000); Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000); Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
• Keywords: クラッシュ症候群 / Fアクチン / DNGR１受容体 / ＤＡＭＰｓ / Ｆアクチン / ＤＮＧＲ１受容体 / DAMPｓ / DNGR1

Outline of Final Research Achievements

The purposes of this study are as follows.①To investigate the F-actin/DNGR-1 signal in the context of systemic acute inflammation following crush injury and to assess the therapeutic effects of anti- F-actin antibody in a rat model of crush injury. ②To evaluate the F-actin/DNGR-1 signal in the patients with systemic inflammation (Trauma and Sepsis). In this study, the administration of anti-Factin antibody did not improve the 7-day survival rate of crush injury rat model. The circulating F-actin levels significantly increased in the patients with sepsis, suggesting that the signal play a role in the pathogenesis of sepsis.