Project/Area Number |
17K07141
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Laboratory animal science
|
Research Institution | Tohoku Medical and Pharmaceutical University (2019-2020) Kanazawa Medical University (2017-2018) |
Principal Investigator |
|
Co-Investigator(Kenkyū-buntansha) |
坂田 ひろみ 金沢医科大学, 医学部, 准教授 (50294666)
|
Project Period (FY) |
2017-04-01 – 2021-03-31
|
Project Status |
Completed (Fiscal Year 2020)
|
Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2019: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2018: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2017: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
|
Keywords | Galectin-9 / 造血幹細胞 / 骨髄 / 炎症 / 好中球 / 血小板 / ガレクチン9 / 好中球分化 |
Outline of Final Research Achievements |
A detailed analysis of bone marrow cells from Gal-9 knock out (KO) mice by flow cytometry revealed that the property of granulocyte-macrophage progenitors (GMPs), which originate from granulocytes and macrophages, in Gal-9 KO mice was higher than those in wild-type (WT) mice. We have previously shown that Gal-9 KO mice exhibit an exacerbation of autoimmune diseases compared to WT mice. Taken together, the exacerbation mechanism by which Gal-9 deficiency leads to exacerbation of murine autoimmune disease model may be partly due to an increase in the number of inflammation-related cells such as neutrophils and macrophages, which are involved in autoimmune diseases. Our current study is a basic research that future clinical application would be expected.
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Academic Significance and Societal Importance of the Research Achievements |
糖鎖は核酸やタンパク質に続く第三の生命鎖と呼ばれ、糖鎖とその認識によるタンパク質の機能修飾及び細胞制御は生命現象を理解する上で無視できない重要な概念の一つとして注目を浴びている。一連の研究でGalectin-9 (Gal-9)がマクロファージ及び好中球の分化や機能を修飾することや、さらに抗血小板凝集作用を明らかにした。本研究課題による成果は、血小板凝集作用におけるGal-9の膜動態制御の解明を目的とした発展的研究へと展開でき、血栓症等の臨床応用も期待できるものとなった。
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