2016 Fiscal Year Final Research Report
Analysis of cellular quality control in liver tissue formation
| Project/Area Number |
26293012
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Partial Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Biological pharmacy
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| Research Institution | Tokyo Medical and Dental University |
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Principal Investigator |
NISHINA Hiroshi 東京医科歯科大学, 難治疾患研究所, 教授 (60212122)
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| Co-Investigator(Kenkyū-buntansha) |
浅岡 洋一 東京医科歯科大学, 難治疾患研究所, 助教 (10436644)
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| Co-Investigator(Renkei-kenkyūsha) |
HIRAYAMA Jun 東京医科歯科大学, 難治疾患研究所, 准教授 (90510363)
MIYAMURA Norio 東京医科歯科大学, 難治疾患研究所, 助教 (10725493)
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| Research Collaborator |
KATADA Toshiaki 東京大学, 大学院薬学研究科, 教授
MIYAJIMA Atsushi 東京大学, 大学分子細胞生物学研究所, 教授
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Keywords | 肝臓 / シグナル / ストレス / 器官形成 |
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| Outline of Final Research Achievements |
The presence of senescent, transformed, or damaged cells can impair tissue function or lead to tumorigenesis. However, how this quality control is regulated remains largely unclear. Here, using in vivo mosaic analysis in mouse liver, we show that YAP activation induced by inactivation of the Hippo pathway specifically in damaged hepatocytes induces their selective elimination. These damaged hepatocytes migrate into the hepatic sinusoids, undergo apoptosis, and are engulfed by Kupffer cells. This involves the activation of CDC42 and Rac to regulate cell migration. Thus, YAP acts as a stress sensor that induces the elimination of injured cells to maintain tissue and organ homeostasis.
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| Free Research Field |
分子細胞生物学
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