Project/Area Number |
15K10167
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Digestive surgery
|
Research Institution | Kyushu University |
Principal Investigator |
IKEGAMI Toru 九州大学, 大学病院, 講師 (80432938)
|
Co-Investigator(Kenkyū-buntansha) |
副島 雄二 九州大学, 大学病院, 助教 (30325526)
池田 哲夫 九州大学, 大学病院, 准教授 (60585701)
調 憲 群馬大学, 大学院医学系研究科, 教授 (70264025)
吉住 朋晴 九州大学, 医学研究院, 准教授 (80363373)
|
Project Period (FY) |
2015-04-01 – 2018-03-31
|
Project Status |
Completed (Fiscal Year 2017)
|
Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2017: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
|
Keywords | 肝再生 / オートファジー / 脂肪肝 / 肝切除 |
Outline of Final Research Achievements |
Murine autophagy suppressed model with Atg5 gene knock out was created using Cre-lox system, followed by hepatic resection and serial sampling of the regenerating liver tissues. It revealed reducedheaptic BrdU intake, accumulated p62 protein (injured protein), lowered serum albumin, p21 protein associated delayed cell cycle turn over with rescued G2 and S, and lower repression of Cyclone D1. These observation was also confirmed using fatty liver autophagy Ko model. In abnormal liver condition including massive heaptectomy, fatty liver, non-alchholic steatosis, diabetes associated liver disease, autophagy is significantly suppressed and smooth regeneration was impaired.
|