Mechanisms of phenotypic changes in macrophages during tissue injury
| Project/Area Number |
17H04068
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Experimental pathology
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| Research Institution | Tokyo University of Pharmacy and Life Science |
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Principal Investigator |
TANAKA MASATO 東京薬科大学, 生命科学部, 教授 (00294059)
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| Co-Investigator(Kenkyū-buntansha) |
大村谷 昌樹 兵庫医科大学, 医学部, 教授 (60398229)
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| Project Period (FY) |
2017-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥17,810,000 (Direct Cost: ¥13,700,000、Indirect Cost: ¥4,110,000)
Fiscal Year 2019: ¥6,890,000 (Direct Cost: ¥5,300,000、Indirect Cost: ¥1,590,000)
Fiscal Year 2018: ¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2017: ¥5,720,000 (Direct Cost: ¥4,400,000、Indirect Cost: ¥1,320,000)
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| Keywords | マクロファージ / 組織傷害 / 形質転換 / 単球 / 炎症 / 転写因子 |
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| Outline of Final Research Achievements |
Macrophages play diverse roles in tissue injury. However, it remains unknown how these macrophages change phenotype according to each phase of tissue injury. This research aimed to reveal mechanisms of phenotypic changes in macrophages during tissue injury. As a result, we demonstrated that two transcriptional factors, c-Maf and Nrf2, determine the phenotype of CD169 macrophages during tissue injury. Furthermore, we identified a novel subpopulation of Ly6C-positive monocytes (Ym1- positive monocytes) in mice. Ym1-positive monocytes are generated in bone marrow during the phase of tissue repair, and contribute to resolution of inflammation and tissue repair in damaged tissues.
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| Academic Significance and Societal Importance of the Research Achievements |
マクロファージは、組織傷害や炎症時に、外界の刺激や環境に素早く対応し、機能的、構造的な変化を起こすことが知られているが、その分子機構は不明な点が多かった。本研究の成果は、特定の転写因子がマクロファージの形質転換に分子スイッチとして働くことを明確に示しており、マクロファージの可塑性および組織傷害の病理を理解する上で有用な知見である。また、得られた知見は将来的に、炎症制御や組織修復促進を目的とした新たな疾患治療法の開発につながる可能性がある。
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Report
(3 results)
Research Products
(19 results)
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[Journal Article] CD169 macrophages regulate immune responses toward particulate materials in the circulating fluid.2018
Author(s)
Deguchi Y, Nishina T, Asano K, Ohmuraya M, Nakagawa Y, Nakagata N, Sakuma T, Yamamoto T, Araki K, Mikami T, Tanaka M, Nakano H.
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Journal Title
Biochem Biophys Res Commun.
Volume: 505
Pages: 453-459
DOI
Related Report
Peer Reviewed / Open Access
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[Journal Article] Tumor Necrosis Factor-Mediated Survival of CD169(+) Cells Promotes Immune Activation during Vesicular Stomatitis Virus Infection.2017
Author(s)
Shinde PV, Xu HC, Maney SK, Kloetgen A, Namineni S, Zhuang Y, Honke N, Shaabani N, Bellora N, Doerrenberg M, Trilling M, Pozdeev VI, van Rooijen N, Scheu S, Pfeffer K, Crocker PR, Tanaka M, Duggimpudi S, Knolle P, Heikenwalder M, Ruland J, Mak TW, Brenner D, Pandyra AA, Hoell JI, Borkhardt A, Haussinger D, Lang KS
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Journal Title
J Virol
Volume: 92
Pages: 01637-01637
DOI
Related Report
Peer Reviewed / Open Access / Int'l Joint Research
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[Journal Article] Depletion of myeloid cells exacerbates hepatitis and induces an aberrant increase in histone H3 in mouse serum2017
Author(s)
Piao X, Yamazaki S, Komazawa-Sakon S, Miyake S, Nakabayashi O, Kurosawa T, Mikami T, Tanaka M, Van Rooijen N, Ohmuraya M, Oikawa A, Kojima Y, Kakuta S, Uchiyama Y, Tanaka M, Nakano H.
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Journal Title
Hepatology
Volume: 65
Pages: 237-252
DOI
NAID
Related Report
Peer Reviewed / Open Access / Int'l Joint Research / Acknowledgement Compliant
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[Journal Article] Salt suppresses IFNgamma inducible chemokines through the IFNgamma-JAK1-STAT1 signaling pathway in proximal tubular cells.2017
Author(s)
Arai Y, Takahashi D, Asano K, Tanaka M, Oda M, Ko SBH, Ko MSH, Mandai S, Nomura N, Rai T, Uchida S, Sohara E.
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Journal Title
Sci Rep
Volume: 7
Pages: 46580-46580
DOI
Related Report
Peer Reviewed / Open Access / Acknowledgement Compliant
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