2012 Fiscal Year Final Research Report
Role of Autophagy and the Molecule Targeting in Sepsis
| Project/Area Number |
22249059
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| Research Category |
Grant-in-Aid for Scientific Research (A)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Emergency medicine
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| Research Institution | Nagoya University |
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Principal Investigator |
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| Project Period (FY) |
2010 – 2012
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| Keywords | 敗血症 / セプシス / オートファジー / 蛋白異化 / 全身性炎症反応症候群 |
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| Research Abstract |
Sepsis, known as a inducer of severe multiple organ diseases, has no established effective treatment except for antibiotics. Sepsis can lead multiple organ failure due to amid acid transformation to acute phase proteins such as inflammatory cytokines. In this study, I have found that some parts of autophagy-related gene family wereincreased at transcriptional and translated levels in the acute terms of sepsis of cultured human vascular endothelial cells and sepsis mouse models. LC3 was activated in particular, and promoted an autophagosome formation. It was concluded that FADD, TAK-1 andtranscriptional activity of NF-κB and AP-1 were significantly related with autophagy acceleration in the cultured human vascular endothelial cells and sepsis mouse model.
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