Signaling mechanisms of chronic inflammation and metabolic diseases
Project/Area Number |
26460571
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Immunology
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Research Institution | Mie University |
Principal Investigator |
OGATA Masato 三重大学, 医学系研究科, 教授 (60224094)
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Project Period (FY) |
2014-04-01 – 2017-03-31
|
Project Status |
Completed (Fiscal Year 2016)
|
Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
|
Keywords | 慢性炎症 / MAPキナーゼ / マクロファージ / 代謝症候群 / p38 / 遺伝子改変マウス |
Outline of Final Research Achievements |
Chronic inflammation and glucose tolerance in high fat diet-induced obesity and NASH model mice were ameliorated in mutant mice in which p38alpha gene was disrupted in hematopoietic cells. As a possible mechanism, involvement of p38alpha in the chemotaxis of proinflammatory M1 macropahges to their target organs was suggested. The p38alpha signaling cascade might be a common therapeutic target of diseases related to chronic inflammation induced by obesity and fatty liver.
|
Report
(4 results)
Research Products
(8 results)
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[Journal Article] Direct visualization of replication dynamics in early zebrafish embryos2016
Author(s)
Kuriya, K., Higashiyama, E., Avsar-Ban, E., Okochi, N., Hattori, K., Ogata, S., Takebayashi, S.I., Ogata, M., Tamaru, Y., Okumura, K
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Journal Title
Bioscience, biotechnology, and biochemistry
Volume: 印刷中
Related Report
Peer Reviewed
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[Journal Article] Direct Visualization of DNA Replication Dynamics in Zebrafish Cells. Zebrafish2015
Author(s)
Kuriya, K., Higashiyama, E., Avsar-Ban, E., Tamaru, Y., Ogata, S., Takebayashi, S., Ogata, M., Okumura, K.
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Journal Title
Zebrafish
Volume: 12
Issue: 5
Pages: 432-439
DOI
Related Report
Peer Reviewed / Open Access
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