Objective： To explore the effects of MG-132 on the expression of VEGF in bronchial epithelial cell line, BEAS- 2B. Methods： Semi-quantitive RT-PCR for VEGF mRNA and enzyme-linked immunosorbent assay （ELISA） for VE...Objective： To explore the effects of MG-132 on the expression of VEGF in bronchial epithelial cell line, BEAS- 2B. Methods： Semi-quantitive RT-PCR for VEGF mRNA and enzyme-linked immunosorbent assay （ELISA） for VEGF protein were performed. Results： MG-132 increased the expression of VEGF mRNA and protein BEAS-2B cells in time-and concentration-dependent manners. After 24-h stimulation, 25 ktmol/L MG-132 increased the maximal levels of VEGF protein in cell-conditioned medium. When the ceUs were stimulated with cycloheximide（CHX） before treatment with MG-132, the MG-132-induced production of VEGF protein was inhibited compared to the unstimulated cells. Supematant of condition-medium treatment with MG-132 enhanced the growth of HUVEC. Conclusion： MG-132 induces VEGF gene expression in human bronchial epithelial cells line, BEAS-2B, and the MG-132-induced expression of VEGF may modulate lung tissue injury due to airway inflammation.展开更多
文摘Objective： To explore the effects of MG-132 on the expression of VEGF in bronchial epithelial cell line, BEAS- 2B. Methods： Semi-quantitive RT-PCR for VEGF mRNA and enzyme-linked immunosorbent assay （ELISA） for VEGF protein were performed. Results： MG-132 increased the expression of VEGF mRNA and protein BEAS-2B cells in time-and concentration-dependent manners. After 24-h stimulation, 25 ktmol/L MG-132 increased the maximal levels of VEGF protein in cell-conditioned medium. When the ceUs were stimulated with cycloheximide（CHX） before treatment with MG-132, the MG-132-induced production of VEGF protein was inhibited compared to the unstimulated cells. Supematant of condition-medium treatment with MG-132 enhanced the growth of HUVEC. Conclusion： MG-132 induces VEGF gene expression in human bronchial epithelial cells line, BEAS-2B, and the MG-132-induced expression of VEGF may modulate lung tissue injury due to airway inflammation.
