Role of oxygen-derived free radicals and BubR1 expression

老龄hAoSMC的BubR1表达和hAoSMC增殖能力明显降低。血管紧张素II和H_2O_2可上调年轻hAoSMC中BubR1的表达，这种上调可被p38 MAPK抑制剂或NADH/NADPH氧化酶抑制剂所抑制。针对BubR1的siRNA抑制了hAoSMC的增殖活性，增加了ROS的产生。这些结果表明，随着增龄hAoSMC的增殖，BubR1mRNA的表达降低。增龄相关的BubR1mRNA的缺失和随后对ROS的反应性降低可能是衰老的hAoSMC增殖能力降低的原因。这些发现表明，随着增龄的增加，BubR1mRNA的表达减少。衰老相关的BubR1的缺失和随后对ROS的反应性受损可能解释了衰老的平滑肌细胞增殖能力降低的原因。

BubR1 expression and hAoSMC proliferative ability were significantly decreased in the aged hAoSMC. Angiotensin II and H2O2 upregulated BubR1 expression in young hAoSMC, and the upregulation was abrogated by a p38 MAPK inhibitor or an inhibitor of the NADH/NADPH oxidase. siRNA against BubR1 reduced proliferative activity and increased ROS production in hAoSMC. These findings demonstrate BubR1 mRNA expression decreases along with proliferation in aged hAoSMC. Aging-related loss of BubR1 and subsequent impairment of reactivity to ROS may explain reduced proliferative capacity of aged smooth muscle cells.These findings demonstrate BubR1 mRNA expression decreases along with proliferation in aged hAoSMC. Aging-related loss of BubR1 and subsequent impairment of reactivity to ROS may explain reduced proliferative capacity of aged smooth muscle cells.