| Project/Area Number |
04454357
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Cerebral neurosurgery
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| Research Institution | NIIGATA UNIVERSITY |
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Principal Investigator |
KOIKE Tetsuo NIIGATA UNIV., MEDICAL HOSPITAL,ASSOCIATE PROFESSOR, 医学部・附属病院, 講師 (20158893)
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| Co-Investigator(Kenkyū-buntansha) |
KAMEYAMA Shigeki NIIGATA UNIV., BRAIN RES.INST., ASSOCIATE PROFESSOR, 脳研究所, 講師 (80186014)
吉田 誠一 新潟大学, 医学部附属病院, 助手 (50174933)
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| Project Period (FY) |
1992 – 1994
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| Project Status |
Completed (Fiscal Year 1994)
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| Budget Amount *help |
¥4,900,000 (Direct Cost: ¥4,900,000)
Fiscal Year 1994: ¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 1993: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 1992: ¥2,400,000 (Direct Cost: ¥2,400,000)
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| Keywords | GLIOMA / ANGIOGENESIS / ENDOTHELIAL CELL / TUMOR NECROSIS FACTOR / lumor necrosls factor / endothelial cells / brain tumor |
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| Research Abstract |
We tried to culture endothelial cells from human glioma specimens using methods described previously. We could obtain primary culture but failde to subculture the cells. Many factors appears to be essential for human endothelialcell culture.
Neovascularization is a prerequisite for glioma growth. Therefore, inhibition of angiogenesis probably lead to control the growth of glioma. We examined whether glioma cells induced angiogenesis using an in vitro co-culture system. Cultured microvascular endothelial cells from Fisher 344 rat brains, rat C6 glioma cells and rat T9 gliosarcoma cells were used in this study. Endothelial cells cultured on type 1 collagen formed capillary-like structures (CS) . C6 glioma cells co-cultured with endothelial cells promoted the formation CS.However, conditioned medium from C6 cells inhibited the proliferation of endothelial cells. T9 cells had a little effect on the formation of CS and no effect on the proliferation of endothelial cells.
We also examined the effects of human tumor necrosis factor (hTNF) -alpha both on the formation of CS and on the proliferation of endothelial cells. hTNF-alpha inhibited the formation of CS induced by C6 glioma cells at a concentration of 100 U/ml as well as the proliferation of endothelial cells at a concentration of 1,000 U/ml.
These results indicate that the ability of promoting angiogenesis is various in each glioma cell and the angiogenesis does not correspond with the proliferation of endothelial cells. It is also revealed that TNF is a capable inhibitor of angiogenesis in gliomas.
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