A new non-invasive in vivo model for evaluation of the adipose inflammatory state.
Project/Area Number |
26660112
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Research Category |
Grant-in-Aid for Challenging Exploratory Research
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Allocation Type | Multi-year Fund |
Research Field |
Food science
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Research Institution | Hiroshima University |
Principal Investigator |
Yanaka Noriyuki 広島大学, 生物圏科学研究科, 准教授 (70346526)
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Project Period (FY) |
2014-04-01 – 2017-03-31
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Project Status |
Completed (Fiscal Year 2016)
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Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2016: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2015: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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Keywords | 肥満 / 脂肪組織 / 炎症 / 非侵襲 / 化学発光 / マクロファージ / 慢性炎症 / serum amyloid A3 / 大腸炎 / DSS大腸炎 / in vivo imaging / CEBP beta / 脂肪細胞 |
Outline of Final Research Achievements |
The infiltration of macrophages into adipose tissue and their interaction with adipocytes are essential for the chronic low-grade inflammation of obese adipose tissue. In this study, we identified the serum amyloid A3 (Saa3) gene that is affected by interaction with macrophages. We showed that the Saa3 promoter in adipocytes actually responds to activated macrophages in a co-culture system. Decreasing C/EBPβ abundance in 3T3-L1 adipocytes or point mutation of C/EBPβ elements suppressed the increased promoter activity in response to activated macrophages, suggesting an essential role of C/EBPβ in Saa3 promoter activation. Bioluminescence based on Saa3 promoter activity in Saa3-luc mice was promoted in obese adipose tissue, showing that Saa3 promoter activity is most likely related to macrophage infiltration. This study suggests that the level of expression of the Saa3 gene could be utilized for the inflammation of obese adipose tissue.
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Report
(4 results)
Research Products
(22 results)
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[Journal Article] New members of the mammalian glycerophosphodiester phosphodiesterase family: GDE4 and GDE7 produce lysophosphatidic acid by lysophospholipase D activity.2015
Author(s)
Ohshima N, Kudo T, Yamashita Y, Mariggio S, Araki M, Honda A, Nagano T, Isaji C, Kato N, Corda D, Izumi T, Yanaka N
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Journal Title
J. Biol. Chem.
Volume: 290
Issue: 7
Pages: 4260-4271
DOI
Related Report
Peer Reviewed
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[Journal Article] Contribution of impaired myofibril and ryanodine receptor function to prolonged low-frequency force depression after in situ stimulation in rat skeletal muscle2015
Author(s)
Watanabe, D., Kanzaki, K., Kuratani, M., Matsunaga, S., Yanaka, N. and Wada, M.
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Journal Title
Journal of Muscle Reearch and Cell Motility
Volume: 印刷中
Issue: 3
Pages: 275-286
DOI
Related Report
Peer Reviewed / Open Access / Acknowledgement Compliant
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