| Project/Area Number |
09670588
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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 |
Gastroenterology
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| Research Institution | Fukuoka University (2000)
Kurume University (1997-1999) |
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Principal Investigator |
SAKISAKA Shotaro School of Medicine, Fukuoka University, Professor, 医学部, 教授 (90158923)
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| Co-Investigator(Kenkyū-buntansha) |
OOISHI Masahito Kurume Univ.Sch.Med.Assistant Prof.(1996-1999), 医学部, 助手 (80289412)
KOGA Hironori Kurume Univ.Sch.Med.Assistant Prof.(1996-1999), 医学部, 助手 (90268855)
HARADA Masaru Kurume Univ.Sch.Med.Assistant Prof.(1996-1999), 医学部, 助手 (00241175)
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| Project Period (FY) |
1997 – 2000
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| Project Status |
Completed (Fiscal Year 2000)
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| Budget Amount *help |
¥2,700,000 (Direct Cost: ¥2,700,000)
Fiscal Year 2000: ¥100,000 (Direct Cost: ¥100,000)
Fiscal Year 1999: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1998: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 1997: ¥800,000 (Direct Cost: ¥800,000)
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| Keywords | VEGF / Liver regeneration / Hepatocyte / in situ hybridization / sinusoidal endothelial cell / 免疫組織化学 / 血管内皮増殖因子 / 激症肝炎 / 劇症肝炎 |
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| Research Abstract |
Vascular endothelial growth factor (VEGF) has been shown to play a major role in angiogenesis, which is essential for both healing of injured tissue and proliferation of carcinoma cells. In this study, we elucidated the expression and role of VEGF in rat liver regeneration after partial hepatectomy. VEGF expression was mainly detected in periportal hepatocytes and reached a maximum level 48 hr after partial hepatectomy by both immunohistochemistry and in situ hybridization. Similarly, immunohistochemistry for Ki-67 showed that the proliferative activity of sinusoidal endothelial cells was highest in the periportal area and reached a maximum level 96 hr after partial hepatectomy. Moreover, neutralization of VEGF significantly inhibited proliferative activity of hepatocytes (P<.0001), as well as sinusoidal endothelial cells (P<.001). Conversely, injection of VEGF singificantly promoted proliferative activity of hepatocytes (P<.0001), as well as sinusoidal endothelial cells (P<.0005). These results suggest that VEGF promotes proliferation of hepatocytes through reconstruction of liver sinusoids by proliferation of sinusoidal endothelial cells. Furthermore, these data point to a new therapeutic strategy, the use of VEGF and other hepatocyte growth factors in fulminant or severe acute hepatitis.
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