2016 Fiscal Year Final Research Report
Pathophysiological Interplay between Liver Fibrosis, Regeneration and Hepatocarcinogenesis from the Viewpoint of Stem/progenitor Cell Differentiation
| Project/Area Number |
25293179
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (B)
|
| Allocation Type | Partial Multi-year Fund |
|---|
| Section | 一般 |
|---|
| Research Field |
Gastroenterology
|
|---|
| Research Institution | Tokai University |
|---|
Principal Investigator |
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
紙谷 聡英 東海大学, 医学部, 准教授 (30321904)
住吉 秀明 東海大学, 医学部, 講師 (60343357)
|
|---|
| Co-Investigator(Renkei-kenkyūsha) |
HOZUMI Katsuto 東海大学, 医学部, 准教授 (30246079)
|
|---|
| Project Period (FY) |
2013-04-01 – 2017-03-31
|
| Keywords | 肝前駆細胞 / 線維化 / 再生 / 発癌 |
|---|
| Outline of Final Research Achievements |
Liver regeneration is severely impaired and hepatocellular carcinoma (HCC) develops frequently in advanced liver fibrosis. The present study was conducted to explore the effects of Jagged1/Notch signal on the induction of hepatic progenitor cells accelerating fibrotic liver regeneration as well as the occurrence of HCC in the fibrotic liver.
Experiments using Jagged1 knockout mice indicated that Jagged1 expressed by activated hepatic stellate cells stimulates Notch2 signal in adjacent hepatocytes, resulting in their dedifferentiation into hepatic progenitor cells. These cells contribute to regeneration of the fibrotic liver. It was also revealed that the Jagged1/Notch signal suppressed the occurrence of diethylnitrosamine-induced HCC.
|
| Free Research Field |
消化器肝臓病学
|
