Project/Area Number |
22591003
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Metabolomics
|
Research Institution | National Defense Medical College |
Principal Investigator |
AYAORI Makoto 防衛医科大学校, 病院, 助教 (70532464)
|
Co-Investigator(Kenkyū-buntansha) |
IKEWAKI Katsunori 防衛医科大学校, 医学教育部医学科専門課程, 教授 (40287199)
HISADA Tetsuya 防衛医科大学校, 医学教育部医学科専門課程, 助教 (70573856)
KONDO Harumi 防衛医科大学校, 医学教育部医学科専門課程, 助教 (80401602)
|
Project Period (FY) |
2010 – 2012
|
Project Status |
Completed (Fiscal Year 2012)
|
Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2012: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2011: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2010: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
|
Keywords | 分子生物学 / HDL / ユビキチン-プロテアソーム系 / コレステロール搬出反応 / コレステロール逆転送 / プロテアソーム阻害薬 / ABCA1/G1 |
Research Abstract |
We demonstrated that ABCA1/G1 was degraded via polyubiquitination in the ubiquitin-proteasome system (UPS). Furthermore, inhibition of the UPS using proteasome inhibitors enhanced both apoA-I- and HDL-mediated cholesterol efflux from macrophages by increasing ABCA1/G1 expressions. Finally, bortezomib, a proteasome inhibitor, promoted overall RCT in vivo in mice. These findings may ultimately provide the basis for a novel therapeutic strategy for atherosclerotic diseases.
|