2013 Fiscal Year Final Research Report
Elucitaion of the mecahisms underlying sepsis deterioration following platelet cell dath
| Project/Area Number |
23592307
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Anesthesiology/Resuscitation studies
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| Research Institution | Kyoto Prefectural University of Medicine |
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Principal Investigator |
NAKAJIMA YASUFUMI 京都府立医科大学, 医学(系)研究科(研究院), 講師 (70326239)
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| Co-Investigator(Kenkyū-buntansha) |
SHIBASAKI Masayuki 京都府立医科大学, 医学研究科, 助教 (20405319)
MIZOBE Toshiki 京都府立医科大学, 医学研究科, 講師 (50239266)
HASHIMOTO Satoru 京都府立医科大学, 医学研究科, 准教授 (90167578)
SAWA Teiji 京都府立医科大学, 医学研究科, 教授 (10206013)
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| Project Period (FY) |
2011 – 2013
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| Keywords | 遺伝子治療 |
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| Research Abstract |
Although platelets play a major role in controlling hemostasis, they also participate in inflammatory regulation. In septic conditions, platelets interact with neutrophils after recognizing pathogen-associated molecular patterns, which subsequently induce neutrophil etosis and release neutrophil extracellular traps (NETs) to efficiently deactivate pathogens. However, if this phenomenon occurs to a large extent, it might lead to organ failure. Here, we tested the hypothesis that controlling platelet cell death can regulate inflammation. We found that LPS and HMGB1 co-incubation accelerated platelet cell death. Knockdown of platelets by p38 MAPK and Bax inhibited this process. Co-incubation of activated platelets and neutrophils resulted in NETs release. Bax knockdown of platelets accelerated this NET release, while p38 MAPK knockdown of platelets inhibited it. The present findings indicate that an optimal platelet activation is necessary to attenuate inflammation.
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Research Products
(26 results)
