Roles of vascular niche in pathophysiology of leukemia and lynphoma
| Project/Area Number |
17K09941
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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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| Research Field |
Hematology
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| Research Institution | Juntendo University |
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Principal Investigator |
Hattori Koichi 順天堂大学, 医学(系)研究科(研究院), 特任先任准教授 (10360116)
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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 |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2019: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2018: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2017: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 細胞・組織 / 生体分子 / シグナル伝達 / 免疫制御学 / 血管内皮 / アンジオクライン因子 / 血液線維素溶解系 |
|---|
| Outline of Final Research Achievements |
In this study, we evaluate the roles of vascular niche including tumor endothelial cells for hematological malignancies (leukemia, lymphoma, and related diseases), and during inflammatory disease progression. Here, we could establish a murine model of hematological malignancies and inflammatory diseases and suggest tissue-specific endothelium establishes specialized vascular niches that deploy sets of fibrinolytic factors matrix metalloproteinases, angiogenic and growth factors like epidermal growth factor like-domain 7 (Egfl7), known as angiocrine factors are distributed by organ-specific endothelium. Additionally, we could show these cues participate actively in the induction, specification, patterning, and guidance of tumor and inflammatory diseases progression and severity, as well as in the maintenance of homeostasis and metabolism through the crosstalk between endothelial cells and mesenchymal or hematological lineage cells driven by cytokines and chemokines.
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| Academic Significance and Societal Importance of the Research Achievements |
本研究の学術的意義として、アンジオクライン因子が、白血病・リンパ腫、そしてこれらの関連疾患の病態において果たす役割を明らかにしたこと、そしてこれを通じて、血管内皮を中心とした複数の系統細胞の相互連関－血管ニッチによるホメオスタシス維持機構をアンジオクラインシステムと捉え、多くの生命現象、疾患病態を血管内皮障害の視点から解明したことが挙げられる。さらに、社会的意義の観点から、本研究で得られた知見を基礎として、白血病・リンパ腫などの血液腫瘍性疾患、炎症性疾患に対するアンジオクライン因子を標的とした新しい分子療法の可能性を研究成果として提示できたことは、社会への還元性を有した重要な研究と評価できる。
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Report
(4 results)
Research Products
(25 results)
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[Journal Article] Pharmacological targeting of plasmin prevents lethality and tissue damage in a murine model of macrophage activation syndrome2017
Author(s)
1.Shimazu H, Munakata S, Tashiro Y, Salama Y, Eiamboonser S, Ohta Y, Onoda H, Tsuda Y, Okada Y, Nakauchi H, Heissig B and Hattori K
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Journal Title
Blood
Volume: 印刷中
Issue: 1
Pages: 59-72
DOI
Related Report
Peer Reviewed / Open Access / Int'l Joint Research / Acknowledgement Compliant
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[Journal Article] Plasminogen activator inhibitor-1 regulates macrophage-dependent postoperative adhesion by enhancing EGF-HER1 signaling in mice.2017
Author(s)
Honjo K, Munakata S, Tashiro Y, Salama Y, Shimazu H, Eiamboonsert S, Dhahri D, Ichimura A, Dan T, Miyata T, Takeda K, Sakamoto K, Hattori K, Heissig B.
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Journal Title
FASEB Journal
Volume: -
Issue: 6
Pages: 2625-2637
DOI
Related Report
Peer Reviewed / Open Access / Int'l Joint Research
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[Presentation] Pharmacological targeting of plasmin prevents lethality and tissue damage in a murine model of macrophage activation syndrome.2017
Author(s)
Shimazu H, Munakata S, Tashiro Y, Salama Y, Eiamboonser S, Ohta Y, Onoda H, Tsuda Y, Okada Y, Nakauchi H, Heissig B and Hattori K.
Organizer
第13回麒麟塾,
Related Report
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