1999 Fiscal Year Final Research Report Summary
The mechanism of sinusoidal endothelial cell apoptosis induced by hydrogen peroxide derived from hepatocytes in hypoxic liver
| Project/Area Number |
10671396
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Anesthesiology/Resuscitation studies
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| Research Institution | AKITA UNIVERSITY |
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Principal Investigator |
SAITO Reijiro Sch. Of Med. Akita Univ. Research Associate, 医学部, 助手 (90272038)
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| Co-Investigator(Kenkyū-buntansha) |
KAWAI Hideki Sch. Of Med. Akita Univ. Research Associate, 医学部, 助手 (20291271)
MINAMIYA Yoshihiro Sch. Of Med. Akita Univ. Associate Prof., 医学部, 助教授 (30239321)
INABA Hideo Sch. Of Med. Akita Univ. Professor, 医学部, 教授 (60159952)
NAKAE Hajime Sch. Of Med. Akita Univ. Research Associate, 医学部, 助手 (10254781)
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| Project Period (FY) |
1998 – 1999
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| Keywords | liver ischemia / hydrogen peroxide / sinusoidal endothelial cell / apoptosis / xanthine oxidase / Bcl-2 / mitochonodria |
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| Research Abstract |
Bcl-2 is now recognized as a potent inhibitor of apoptotic cell death. In this study, we investigated the mechanism of sinusoidal endothelial cell apoptosis induced by hydrogen and liver protection using Bcl-2. Here we report that hypoxia induces xanthine oxidase-dependent hydrogen peroxide production in hepatocytes, and that this diffuses into sinusoidal endothelial cells and induces selective sinusoidal endothelial cells apoptosis in the blood-perfused rat liver. On the other hand, we reported that Bcl-2 is located in the mitochondria, endoplasmic reticulum, and nuclear membrane and that Bcl-2 is expressed in normal rat liver, and locatedpredominantly in the inner membrane and crista rather than in the outer membrane of mitochondria.
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