Immunohistochemical study of relationship between autophagy marker LC3 and nutritional state in human livers.
| Project/Area Number |
24590851
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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 |
Legal medicine
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| Research Institution | The University of Tokyo |
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Principal Investigator |
NAKAJIMA Makoto 東京大学, 医学(系)研究科(研究院), 技術専門員 (70396696)
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| Co-Investigator(Kenkyū-buntansha) |
YOSHIDA Kenichi 東京大学, 大学院医学系研究科, 教授 (40166947)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥5,460,000 (Direct Cost: ¥4,200,000、Indirect Cost: ¥1,260,000)
Fiscal Year 2014: ¥390,000 (Direct Cost: ¥300,000、Indirect Cost: ¥90,000)
Fiscal Year 2013: ¥390,000 (Direct Cost: ¥300,000、Indirect Cost: ¥90,000)
Fiscal Year 2012: ¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
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| Keywords | オートファジー / 肝臓 / LC3 / 免疫染色 / Autophagy / 飢餓 / 脂肪肝 / ＬＣ3 |
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| Outline of Final Research Achievements |
Microｔubule-associated protein 1 light chain 3 (LC3) immunohistochemistry reproducibly delineated puncta in normal human liver, which were preferentially located around the central venal zone. The extent of LC3 immunostaining reduced as progressing steatosis. Double immunofluorescence for Adipose differentiation -related protein (ADRP) and LC3 demonstreted that positive area of the twe protein have inverse relationship, as well as that they are co-localization on the membrane of small lipid droplets ( LDs) but not of large LDs.
These findings suggest that impaired autophagy promotes steatosis and that autophagy may be implicated in LD turnover.
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Report
(4 results)
Research Products
(6 results)
