Role of oxygen-derived free radicals and BubR1 expression

老年hAoSMC中BubR1的表达和增殖能力明显降低。血管紧张素II和H2O2上调了年轻型hAoSMC中BubR1的表达，而上调被p38 MAPK抑制剂或NADH/NADPH氧化酶抑制剂所消除。抗BubR1的siRNA降低了hAoSMC的增殖活性，增加了ROS的产生。这些结果表明，在老年hAoSMC中，BubR1 mRNA的表达随细胞增殖而降低。衰老相关的BubR1缺失和随后对ROS的反应性损伤可能解释了衰老平滑肌细胞增殖能力降低的原因。这些结果表明，在老年hAoSMC中，BubR1 mRNA的表达随细胞增殖而降低。衰老相关的BubR1缺失和随后对ROS的反应性损伤可能解释了衰老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.