Phd/VHL/HIF-1制御系を介した白血病幹細胞の代謝特性解明と標的療法開発

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Author: 田久保, 圭誉

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Publication date: 2014

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Note (General)：: type:text代謝解析から造血幹細胞ニッチの新たな制御機構としてピルビン酸脱水素酵素リン酸化酵素を, 白血病幹細胞ニッチの新規シグナルとしてIL-2/CD25シグナルを見出した。前者からは, 代謝制御を標的とした感染制御や造血系抗老化技術につながることが期待され, 後者からは未だ根絶が難しい慢性...

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科研費研究者番号 : 50502788

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Material Type: 文書・図像類
Title: Phd/VHL/HIF-1制御系を介した白血病幹細胞の代謝特性解明と標的療法開発
Author/Editor: 田久保, 圭誉
Author Heading: 田久保, 圭誉
Publication Date: 2014
Publication Date (W3CDTF): 2014
Alternative Title: Phd/VHL/HIF-1 セイギョケイオカイシタハッケツビョウカンサイボウノタイシャトクセイカイメイトヒョウテキリョウホウカイハツ
Phd/VHL/HIF-1 seigyokei o kaishita hakketsubyo kansaibo no taisha tokusei kaimei to hyoteki ryoho kaihatsu
Elucidation of metabolic phenotypes of LICs and development of targeting therapy against LICs through Phd/VHL/HIF-1 regulatory system
Periodical title: 科学研究費補助金研究成果報告書
Text Language Code: jpn
eng
Subject Heading: 造血幹細胞,白血病幹細胞,幹細胞ニッチ,メタボロミクス
Target Audience: 一般
Note (General): type:text
代謝解析から造血幹細胞ニッチの新たな制御機構としてピルビン酸脱水素酵素リン酸化酵素を, 白血病幹細胞ニッチの新規シグナルとしてIL-2/CD25シグナルを見出した。前者からは, 代謝制御を標的とした感染制御や造血系抗老化技術につながることが期待され, 後者からは未だ根絶が難しい慢性骨髄性白血病幹細胞に対する新しい治療法が開発されることが期待される。 (1) We performed metabolomic analysis in hematopoietic stem cells (HSCs) and found that HSCs generate adenosine-5'-triphosphate by anaerobic glycolysis through a pyruvate dehydrogenase kinase (Pdk)-dependent mechanism. Loss of both Pdk isozymes attenuated HSC phenotypes including cell cycle. Thus, glycolytic metabolic status governed by Pdk acts as a cell cycle checkpoint that modulates HSCs. (2) Using a CML-like mouse model of myeloproliferative disease, we demonstrate that CML LICs can be divided into CD25(+)FcεRIα(-) Lineage marker (Lin)(-) Sca-1(+)c-Kit(+) (F(-)LSK) cells and CD25(-)F(-)LSK cells. The CD25(+)F(-)LSK cells had multilineage differentiation capacity, with a preference toward cytokine-producing mast cell commitment. The CD25(+)F(-)LSK cells exhibited higher LIC capacity. Our findings suggest that interleukin-2 derived from the microenvironment and CD25 expressed on CML LICs constitute a novel signaling axis that could be preferentially targeted in therapy for CML.
研究種目 : 若手研究(A) 研究期間 : 2011～2014 課題番号 : 23689049 研究分野 : 血液学
Access Restrictions: 限定公開
Related Material: 科研費研究者番号 : 50502788
Data Provider (Database): 国立情報学研究所 : 学術機関リポジトリデータベース（IRDB）（機関リポジトリ）
https://irdb.nii.ac.jp
Original Data Provider (Database): 慶應義塾大学 : 慶應義塾大学学術情報リポジトリ