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Effect of Anti-vascular Endothelial Growth Factor Antibody on the Survival of Cultured Retinal Ganglion Cells

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Purpose: To investigate the effects of anti-vascular endothelial growth factor (VEGF) antibody on the survival ofretinal ganglion cell (RGC)-5 cells differentiated with staurosporine under oxidative stress. Methods: We used real-time polymerase chain reaction and Western blot to confirm the expression of VEGF,VEGF receptor (VEGFR)-1 and VEGFR-2 in RGC-5 cells differentiated with staurosporine for 6 hours. The differentiatedRGC-5 cells were treated with 800 μM hydrogen peroxide (H2O2) for 24 hours to induce oxidativestress. Then, the survival rate of RGC-5 was confirmed by lactate dehydrogenase assay at each concentration(0, 0.01, 0.1, and 1 mg) using bevacizumab as the anti-VEGF antibody. The expression of VEGF, VEGFR-1,and VEGFR-2 was confirmed using real-time polymerase chain reaction. Results: VEGF, VEGFR-1, and VEGFR-2 were all expressed in differentiated RGC-5 cells. When RGC-5 cellswere simultaneously treated with bevacizumab and 800 μM H2O2, survival of RGC-5 decreased with bevacizumabconcentration. VEGF expression in RGC-5 cells increased with increasing concentration of bevacizumab. Similar patterns were observed for VEGFR-1 and VEGFR-2, but the degree of increase was smaller thanthat for VEGF. Conclusions: When bevacizumab was administered to differentiated RGC-5 cells, the cell damage caused byoxidative stress increased. Therefore, given these in vitro study results, caution should be exercised with bevacizumabtreatment.

Abstract

Purpose: To investigate the effects of anti-vascular endothelial growth factor (VEGF) antibody on the survival ofretinal ganglion cell (RGC)-5 cells differentiated with staurosporine under oxidative stress. Methods: We used real-time polymerase chain reaction and Western blot to confirm the expression of VEGF,VEGF receptor (VEGFR)-1 and VEGFR-2 in RGC-5 cells differentiated with staurosporine for 6 hours. The differentiatedRGC-5 cells were treated with 800 μM hydrogen peroxide (H2O2) for 24 hours to induce oxidativestress. Then, the survival rate of RGC-5 was confirmed by lactate dehydrogenase assay at each concentration(0, 0.01, 0.1, and 1 mg) using bevacizumab as the anti-VEGF antibody. The expression of VEGF, VEGFR-1,and VEGFR-2 was confirmed using real-time polymerase chain reaction. Results: VEGF, VEGFR-1, and VEGFR-2 were all expressed in differentiated RGC-5 cells. When RGC-5 cellswere simultaneously treated with bevacizumab and 800 μM H2O2, survival of RGC-5 decreased with bevacizumabconcentration. VEGF expression in RGC-5 cells increased with increasing concentration of bevacizumab. Similar patterns were observed for VEGFR-1 and VEGFR-2, but the degree of increase was smaller thanthat for VEGF. Conclusions: When bevacizumab was administered to differentiated RGC-5 cells, the cell damage caused byoxidative stress increased. Therefore, given these in vitro study results, caution should be exercised with bevacizumabtreatment.

참고문헌 (22)

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