Project/Area Number |
13670494
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Gastroenterology
|
Research Institution | The University of Tokyo |
Principal Investigator |
TOMIYA Tomoaki The University of Tokyo, Faculty of Medicine, Research Associate, 医学部附属病院, 助手 (90227637)
|
Co-Investigator(Kenkyū-buntansha) |
YANASE Mikio The University of Tokyo, Faculty of Medicine, Research Associate, 医学部附属病院, 助手 (50334397)
ARAI Masahiro The University of Tokyo, Faculty of Medicine, Research Associate, 医学部附属病院, 助手 (60271566)
IKEDA Hitoshi The University of Tokyo, Faculty of Medicine, Research Associate, 医学部附属病院, 助手 (80202422)
|
Project Period (FY) |
2001 – 2002
|
Project Status |
Completed (Fiscal Year 2002)
|
Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2002: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 2001: ¥2,900,000 (Direct Cost: ¥2,900,000)
|
Keywords | Hepatocytes / proliferation / HGF / TGFα / functions |
Research Abstract |
While differentiated cellular functions are thought to be suppressed during cell proliferation, recent studies have revealed that several mitogens stimulate protein production in hepatocytes as well as proliferation. We studied the significance of intracellular signal transduction during proliferation and protein production in hepatocytes stimulated by hepatocyte growth factor (HGF) and transforming growth factor α (TGFα). In hepatocytes cultured at low density, the EGF/TGFα receptor activation and the PI3K signaling pathway, perhaps through the activation of p70S6 kinase, may contribute to the up-regulation of DNA synthesis by HGF. This growth factor also stimulates albumin production in hepatocytes cultured at high density, also via the activation of the PI3K pathway but independent of TGFα These results suggest that, depending on the physiological conditions, PI3K pathways can mediate either cell proliferation or protein production in hepatocytes stimulated by HGF.
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