Objective: Neovascularization of tumor is a complex process. In this study, we aimed to reveal whether the bone marrow-originated endothelial progenitor cells (EPCs) contributed to neovasculature in tumor and the angi...Objective: Neovascularization of tumor is a complex process. In this study, we aimed to reveal whether the bone marrow-originated endothelial progenitor cells (EPCs) contributed to neovasculature in tumor and the angiogenesis-associ-ated factors, VEGF and B-FGF, enhanced this process. Methods: We had established a mouse model, which were deprived of bone marrow by radiation and transplanted with bone marrow of syngenetic GFP (Green Fluorescence Protein)-transgened mice, then implanted Lewis cells. Immunohistochemical and immunoflourensence proved the EPCs location in tumors by indentifying colocalization of GFP expression in cells staining with endothelial progenitor cell markers, CD 133, ICAM-1, CD31. The growth statue and MVD of tumor was observed after injection of VEGF or B-FGF. ICAM-1 and VE-cadherin in tumor were detected by Western blot. Results: By immunohistochemical and immunoflourensence, we proved part of bone marrow precursors located in area of tumor angiogenesis and VEGF or B-FGF increased the MVD of tumor. In Western blot, it was found and VEGF or B-FGF up-regulate the expression of ICAM-1, VE-Cadherin. Conclusion: Bone marrow-derived endothelial progenitor cell seem to be recruited in neovasculature induced by tumor. VEGF and B-FGF are key regulators of this process.展开更多
基金the National Key Project of Scientific and Technical Supporting Programs Funded by Ministry of Science & Tech-nology of China (No. 2006BAI02A05)
文摘Objective: Neovascularization of tumor is a complex process. In this study, we aimed to reveal whether the bone marrow-originated endothelial progenitor cells (EPCs) contributed to neovasculature in tumor and the angiogenesis-associ-ated factors, VEGF and B-FGF, enhanced this process. Methods: We had established a mouse model, which were deprived of bone marrow by radiation and transplanted with bone marrow of syngenetic GFP (Green Fluorescence Protein)-transgened mice, then implanted Lewis cells. Immunohistochemical and immunoflourensence proved the EPCs location in tumors by indentifying colocalization of GFP expression in cells staining with endothelial progenitor cell markers, CD 133, ICAM-1, CD31. The growth statue and MVD of tumor was observed after injection of VEGF or B-FGF. ICAM-1 and VE-cadherin in tumor were detected by Western blot. Results: By immunohistochemical and immunoflourensence, we proved part of bone marrow precursors located in area of tumor angiogenesis and VEGF or B-FGF increased the MVD of tumor. In Western blot, it was found and VEGF or B-FGF up-regulate the expression of ICAM-1, VE-Cadherin. Conclusion: Bone marrow-derived endothelial progenitor cell seem to be recruited in neovasculature induced by tumor. VEGF and B-FGF are key regulators of this process.
