Role of PAD4 for inflammatory diseases and neutrophil extracellular traps
Project/Area Number |
25461494
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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 |
Collagenous pathology/Allergology
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Research Institution | National Cancer Center Japan |
Principal Investigator |
Nakashima Katsuhiko 国立研究開発法人国立がん研究センター, 研究所, 研究員 (90528035)
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Project Period (FY) |
2013-04-01 – 2016-03-31
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Project Status |
Completed (Fiscal Year 2015)
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Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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Keywords | シトルリン化 / 炎症 / PAD4 |
Outline of Final Research Achievements |
Peptidylarginine deiminase 4 (PAD4) is a nuclear-localized citrullination enzyme and transcription regulator through citrullination of histone H3. It has been reported that PAD4 is essential for neutrophil extracellular traps (NETs) which is a event on bacterial infection and inflammation. In this study, we examined the role of PAD4 on acute lung injury (ALI) using PAD4-deficient mouse. The results showed expression of inflammatory cytokines, IL-6, TNF-alpha, MCP-1, and IL-1beta, were suppressed by PAD4-deficiency. Next, we assessed the role of PAD4 on macrophage differentiation of M1 cells, mouse myelocytic leukemia cells. Ectopic expression of PAD4 but not mutant PAD4 in M1 cells induced apoptosis during IL-6 treatment of M1 cells. In addition, c-myc expression on IL-6 treatment is suppressed by ectopic expression of PAD4 but not mutant PAD4. These results suggested that PAD4 plays important roles on inflammatory response, especially ALI.
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Report
(4 results)
Research Products
(9 results)
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[Journal Article] MafB promotes atherosclerosis by inhibiting foam-cell apoptosis2014
Author(s)
Hamada M, Nakamura M, Tran MT, Moriguchi T, Hong C, Ohsumi T, Dinh TT, Kusakabe M, Hattori M, Katsumata T, Arai S, Nakashima K, Kudo T, Kuroda E, Wu CH, Kao PH, Sakai M, Shimano H, Miyazaki T, Tontonz P, Takahashi S
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Journal Title
Nat Commun
Volume: 5
Issue: 1
Pages: 3147-3147
DOI
Related Report
Peer Reviewed / Open Access
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