2020 Fiscal Year Final Research Report
Non-renal and enzymatic regulation of neutrophils in inflammatory kidney diseases
| Project/Area Number |
18K08232
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Review Section |
Basic Section 53040:Nephrology-related
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| Research Institution | The University of Tokyo |
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Principal Investigator |
Nishi Hiroshi 東京大学, 医学部附属病院, 講師 (90784174)
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| Project Period (FY) |
2018-04-01 – 2021-03-31
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| Keywords | 好中球 / 腎臓 / 炎症 / 神経 / 血管生物学 / 白血球 / 血栓 |
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| Outline of Final Research Achievements |
Neutrophils accumulate and promote tissue damage in the kidneys during the active and acute stages of various inflammatory renal diseases. Therefore, we sought methods to regulate neutrophil activation from outside the kidney and intracellular space.
As extra-renal stimuli, we spoted unknown function of neurotransmitter molecules. Our studies have shown that some of these neurotransmitters may act protectively against inflammation.
As intra-cellular signaling, we focus on the phosphorylation signal pathway stimulated by migratory factors. In particular, a number of kinases activated by DNA and RNA is required for reactive oxidative species production, adhesion to vascular endothelium, and vascular migration, which was shown to play a role to interact with cytoskeleton and mediated vascular inflammation.
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| Free Research Field |
腎臓内科学
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| Academic Significance and Societal Importance of the Research Achievements |
好中球は種々の炎症性腎疾患の活動期及び急性期の腎に蓄積し，脱顆粒や活性酸素放出などのメカニズムを通じて，組織障害を助長すると考えられている．そこで，疾患活動期に注目して，特に炎症性腎疾患における腎外・細胞内からの好中球制御する手段を模索してきた．
今後，好中球内の分子を標的にするような低分子化合物や上流シグナル遮断が可能になれば，炎症性腎疾患の治療手段として大いに期待できる．
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