Department of Biochemistry and Molecular Biology, Aging-associated Vascular Disease Research Center, College of Medicine, Yeungnam University, Daegu, Republic of Korea.
FEBS Lett. 2011 Nov 16;585(22):3569-76. doi: 10.1016/j.febslet.2011.10.022. Epub 2011 Oct 20.
Aurora B kinase (Aurora-B) functions in chromosome segregation and cleavage of polar spindle microtubules. However, its role in cellular senescence remains elusive. Here, we investigated Aurora-B effects on cellular senescence in human fibroblasts and endothelial cells. Aurora-B levels were reduced during replicative senescence and premature senescence by adriamycin. Aurora-B overexpression in old cells partially reversed senescence phenotypes. In contrast, Aurora-B down-regulation accelerated cellular senescence. p53 knockdown but not p16 knockdown inhibited cellular senescence by Aurora-B reduction. These results suggest that Aurora-B might function in the regulation of cellular senescence of human primary cells via a p53-dependent pathway.
极光 B 激酶（Aurora-B）在染色体分离和极性纺锤体微管的切割中起作用。然而，其在细胞衰老中的作用仍不清楚。在这里，我们研究了 Aurora-B 对人成纤维细胞和内皮细胞衰老的影响。在复制性衰老和阿霉素诱导的早衰过程中，Aurora-B 水平降低。在衰老细胞中过表达 Aurora-B 部分逆转了衰老表型。相反，Aurora-B 的下调加速了细胞衰老。p53 敲低而非 p16 敲低抑制 Aurora-B 减少引起的细胞衰老。这些结果表明，Aurora-B 可能通过 p53 依赖的途径在人原代细胞衰老的调控中发挥作用。
