2017 Fiscal Year Final Research Report
Development of new method for measuring mitochondrial activity of dendritic cells
Project/Area Number |
16K19196
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Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Multi-year Fund |
Research Field |
Laboratory medicine
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Research Institution | Kyushu University |
Principal Investigator |
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Project Period (FY) |
2016-04-01 – 2018-03-31
|
Keywords | ミトコンドリア |
Outline of Final Research Achievements |
Sepsis is a major cause of morbidity and mortality in seriously ill patients and mitochondrial dysfunction is associated with poor outcomes in septic patients. We identified p32/C1QBP/HABP1 as a regulator of IL-6 production in response to lipopolysaccharide (LPS). LPS induced IL-6 overproduction in p32 deficient mouse embryonic fibroblasts (MEFs) through activating transcription factor (ATF) 4 dependent pathways. Using a LPS-induced endotoxin shock model, mice with p32 ablation in myeloid cells showed increased lethality and overproduction of IL-6. We constructed new system to measure real-time metabolic activity of dendritic cells. We demonstrated that p32/C1qbp, which functions as a multifunctional chaperone protein of mitochondria, supports not only mitochondrial metabolism but also DC maturation.
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Free Research Field |
臨床検査医学
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