| Budget Amount *help |
¥3,050,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥150,000)
Fiscal Year 2007: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2006: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 2005: ¥1,700,000 (Direct Cost: ¥1,700,000)
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| Research Abstract |
Interleukin (IL)-6 and granulocyte-stimulating factor (G-CSF) are multifunctional regulator of immune response, hematopoiesis and acute phase reaction, and suppose to have the direct and/or indirect effect to the cancer cells. Recently, it has been reported that serum levels of interleukin-6 (IL-6) and expression in cancer tissues are correlated with the prognosis in various cancer patients. In this present study, we investigated that whether the proliferation and angiogenesis potential were influenced with IL-6 or G-CSF treatment in endothelial cells. Endothelial cell lines, HUV-EC-C (human, vascular endothelium, umbilical vein) and MS1 VEGF (Mouse, Pancreas vein, SV40 transformed; infected with a vector for VEGF) were used.
Proliferation : MS1 VEGF was observed higher potential of proliferation than HUV-EC-C. IL-6 and G-CSF did not enhance the proliferation of HUV-EC-C and MS1 VEGF.
Angiogenesis Assay : This angiogenesis assay represents a model of angiogenesis in which the induction o
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r inhibition of tube formation. Assay instructions ; 1 : Labtec II chamber slides was used, 2 : Dispense 200μL fibrinogen solution into the chamber slides, 3 : Add 13312 L per well thrombin to the chamber, 4 : Place slides at 37℃ for 60 min to polymerize, 5 : HUV-EC-C and MS1 VEGF were resuspend at a final concentration of 5 X 10^4 cells-mL in media, 6 : Add 1000 /μL HUV-EC-C and MS1 VEGF in well in chamber slides, 7 : Add 200μL per well fibrinogen in chamber slides, 8 : Add 133 μL per well thrombin in chamber slide, 8 : Place in 37℃ 5%CO_2 incubator.
Angiogenesis: HUV EV-C was observed angiogenesis in angiogenesis assay, but MS1 VEGF which producted high VEGF was not observed angiogenesis in angiogenesis assay. Angiogenesis of HUV-EC-C was enhanced by bFGF 50μg/ml and/or PMA 50μg/m. Otherwise, Angiogenesis of MS1 VEGF was not enhanced by bFGF 50μg/ml and/or PMA 50μg/m.
Conclusion: VEGF enhanced the proliferation of endothelial cells. MS1 VEGF which products high VEGF has high potential of proliferation, but MS1 VEGF showed poor angiogenesis (capillary formation). VEGF enhanced proliferation but not angiogenesis (capillary formation) of endothelial cells. So VEGF cause the immature vessels in tumor tissue. Less
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