OBJECT: Glioblastomas multiforme (GBM) contain a higher number of alpha-smooth muscle actin (SMA)-positive vascular smooth muscle cells (VSMCs) than those in the respective normal neuronal tissue. The role of VSMCs during angiogenesis is unclear, and it is also uncertain whether and to what extent angiogenic factors might be involved in GBM VSMCs. In GBMs, the contribution of VSMCs in angiogenesis accompanying endothelial proliferation and the correlation of VSMC proliferation with vascular endothelial growth factor (VEGF) expression were examined using an immunohistochemical method. METHODS: The examined material, including surrounding brain tissue, came from 12 cases (6 men and 6 women) with classic GBM. Microvessel densities (MVDs) of CD31-immunoreactive vessels (CD31-MVD) and SMA-immunoreactive vessels (SMA-MVD) were obtained in areas selected from white matter, boundary, tumor (concentrated area of tumor cells), and perinecrosis. Subsequently, the SMA-MVD/CD31-MVD (SMA/CD31) rate, representing the percentage of vessels with VSMCs in the region, was calculated in each area. The VEGF immunoreactivity of tumor cells was examined, and cases were divided into 2 groups: < 30% VEGF expression of tumor cells (low VEGF group) and > 30% VEGF expression of tumor cells (high VEGF group). RESULTS: The SMA/CD31 rate of the boundary was significantly lower than that of the tumor (p < 0.005) and perinecrosis (p < 0.001). The SMA/CD31 rate of the high VEGF group was significantly higher than that of the low VEGF group (p < 0.05) in the tumor. CONCLUSIONS: In GBMs, the transformation and proliferation of VSMCs may accompany neovascularization and may also be induced by angiogenic factors.
OBJECT: Glioblastomas multiforme (GBM) contain a higher number of alpha-smooth muscle actin (SMA)-positive vascular smooth muscle cells (VSMCs) than those in the respective normal neuronal tissue. The role of VSMCs during angiogenesis is unclear, and it is also uncertain whether and to what extent angiogenic factors might be involved in GBM VSMCs. In GBMs, the contribution of VSMCs in angiogenesis accompanying endothelial proliferation and the correlation of VSMC proliferation with vascular endothelial growth factor (VEGF) expression were examined using an immunohistochemical method. METHODS: The examined material, including surrounding brain tissue, came from 12 cases (6 men and 6 women) with classic GBM. Microvessel densities (MVDs) of CD31-immunoreactive vessels (CD31-MVD) and SMA-immunoreactive vessels (SMA-MVD) were obtained in areas selected from white matter, boundary, tumor (concentrated area of tumor cells), and perinecrosis. Subsequently, the SMA-MVD/CD31-MVD (SMA/CD31) rate, representing the percentage of vessels with VSMCs in the region, was calculated in each area. The VEGF immunoreactivity of tumor cells was examined, and cases were divided into 2 groups: < 30% VEGF expression of tumor cells (low VEGF group) and > 30% VEGF expression of tumor cells (high VEGF group). RESULTS: The SMA/CD31 rate of the boundary was significantly lower than that of the tumor (p < 0.005) and perinecrosis (p < 0.001). The SMA/CD31 rate of the high VEGF group was significantly higher than that of the low VEGF group (p < 0.05) in the tumor. CONCLUSIONS: In GBMs, the transformation and proliferation of VSMCs may accompany neovascularization and may also be induced by angiogenic factors.
Authors: Marco Tafani; Maura Di Vito; Alessandro Frati; Laura Pellegrini; Elena De Santis; Giovanni Sette; Adriana Eramo; Patrizio Sale; Emanuela Mari; Antonio Santoro; Antonino Raco; Maurizio Salvati; Ruggero De Maria; Matteo A Russo Journal: J Neuroinflammation Date: 2011-04-13 Impact factor: 8.322
Authors: Lucio Díaz-Flores; Ricardo Gutiérrez; Miriam González-Gómez; María-Del-Pino García; Lucio Díaz-Flores; Ibrahim González-Marrero; Julio Ávila; Pablo Martín-Vasallo Journal: Cells Date: 2021-10-01 Impact factor: 6.600
Authors: Julia Onken; Peter Vajkoczy; Robert Torka; Claudia Hempt; Victor Patsouris; Frank L Heppner; Josefine Radke Journal: Oncotarget Date: 2017-06-13