Project/Area Number |
11470132
|
Research Category |
Grant-in-Aid for Scientific Research (B).
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Gastroenterology
|
Research Institution | Osaka University |
Principal Investigator |
HAYASHI Norio Osaka University Graduate School of Medicine, Professor, 医学系研究科, 教授 (00144478)
|
Co-Investigator(Kenkyū-buntansha) |
MOCHIZUKI Kiyosi Osaka University Hospital, Clinical Staff, 医学部・附属病院, 医員
HIRAMATSU Naoki Osaka University Hospital, Clinical Staff, 医学部・附属病院, 医員
SASAKI Yutaka Osaka University Graduate School of Medicine, Associate Professor, 医学系研究科, 助教授 (70235282)
OKAWA Kazuyoshi Osaka University Hospital, Clinical Staff, 医学部・附属病院, 医員
|
Project Period (FY) |
1999 – 2000
|
Project Status |
Completed (Fiscal Year 2000)
|
Budget Amount *help |
¥14,100,000 (Direct Cost: ¥14,100,000)
Fiscal Year 2000: ¥4,900,000 (Direct Cost: ¥4,900,000)
Fiscal Year 1999: ¥9,200,000 (Direct Cost: ¥9,200,000)
|
Keywords | Hepatitis C virus / Apoptosis / Cell cycle / Hepatocyte / Core / Microarray / 樹状細胞 / IL-12 / 抗アポト-シス |
Research Abstract |
To investigate influence of hepatitis C virus (HCV) infection on hepatocyte, we established several permanent hepatocyte clones that express HCV core gene. Microarray analysis of these clones revealed a couple of gene of which expression was modulated in HCV core-expressing clones. We applied Nothern blot analysis to confirm 2 genes of which expression was downrgulated as well as 3 genes of which expression was upregulated in HCV core-expressing clones. We are currently analyzing the role of these genes in hepatocytes. We also investigated the effect of HCV core expression on apoptosis as well as cell proliferation. Expression of HCV core gene did not affect apoptosis, but significantly retarded proliferation of hepatocyte by inhibiting G1/S transition. These results suggest that infection of HCV inhibits hepatocyte proliferation but does not affect apoptosis of hepatocytes, raising the possibility that HCV-infected hepatocytes can be eradicated by apoptotic stimuli.
|