Regulation of inflammation associated with cell death
| Project/Area Number |
24390100
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Partial Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Experimental pathology
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| Research Institution | Toho University (2014)
Juntendo University (2012-2013) |
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Principal Investigator |
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥18,720,000 (Direct Cost: ¥14,400,000、Indirect Cost: ¥4,320,000)
Fiscal Year 2014: ¥5,460,000 (Direct Cost: ¥4,200,000、Indirect Cost: ¥1,260,000)
Fiscal Year 2013: ¥6,240,000 (Direct Cost: ¥4,800,000、Indirect Cost: ¥1,440,000)
Fiscal Year 2012: ¥7,020,000 (Direct Cost: ¥5,400,000、Indirect Cost: ¥1,620,000)
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| Keywords | アポトーシス / ネクローシス / cFLIP / 肝炎 / 腸炎 / 皮膚炎 / 骨髄移植 / TNFa / ケラチノサイトサイト / TNFR1 / 分化マーカー / 増殖因子 / 表皮 / 貪食細胞 / 炎症 / インターロイキン6 / クッパー細胞 / DAMPs / 単球 / c-FLIP / ネクロプトーシス |
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| Outline of Final Research Achievements |
To investigate a role for cFLIP in tissue homeostasis, we generated conditional cFLIP-deficient mice. Hepatocyte-, intestinal epithelial cell-, and epidermis-specific cFLIP-deficient mice died perinatally due to enhanced apoptosis or necroptosis of respective tissues, suggesting that cFLIP plays an essential role in maintaining tissue homeostasis. We also generated mice, in which expressions of cFLIP in hepatocytes were decreased (cFLIPHeplow mice) to half compared to those of wild-type mice. Upon TNFα injection, cFLIPHeplow mice spontaneously developed transient and mild hepatitis. We next investigated whether Kupffer cells or infiltrated monocytes were required for suppression of inflammation associated with cell death. Depletion of infiltrated monocytes, but not Kupffer cells resulted in exacerbation of hepatitis along with strong elevation of inflammatory cytokines, suggesting that infiltrated monocytes, but not Kupffer cells play a crucial role in suppression of inflammation.
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Report
(4 results)
Research Products
(43 results)
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[Journal Article] Disruption of Tumor Necrosis Factor Receptor Associated Factor 5 Exacerbates Pressure Overload Cardiac Hypertrophy and Fibrosis.2014
Author(s)
Bian, Z., Dai, J., Nakano, H., Guan, H., Yuan, Y., Gan, L., Zhou, H., Zong, J., Zhang, Y., Li, F., Yan, L., Shen, D., Li, H., and Tang, Q.
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Journal Title
J Cell Biochem
Volume: 115
Issue: 2
Pages: 349-358
DOI
Related Report
Peer Reviewed
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[Journal Article] Interleukin-11 Links Oxidative Stress and Compensatory Proliferation2012
Author(s)
Nishina T, Komazawa-Sakon S, Yanaka S, Zheng X, Palo J, Kojima Y, Yamashina S, Sano E, Putoczki T, Doi T, Ueno T, Ezaki J, Ushio H, Ernst M, Kouhei T, Okamura K, Nakano H
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Journal Title
Science Signal
Volume: 5
Issue: 207
DOI
Related Report
Peer Reviewed
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