Takauji Yuki, Wada Takumi, Takeda Asuka, Kudo Ikuru, Miki Kensuke, Fujii Michihiko, Ayusawa Dai
Graduate School of Nanobioscience, Yokohama City University, 22-2 Seto, Kanazawa-ku, Yokohama, Kanagawa 236-0027, Japan.
Ichiban Life Corporation, 1-1-7 Horai-cho, Naka-ku, Yokohama, Kanagawa 231-0048, Japan.
Sci Rep. 2016 Jan 5;6:18722. doi: 10.1038/srep18722.
Cellular senescence or its equivalence is induced by treatment of cells with an appropriate inducer of senescence in various cell types. Mild restriction of cytoplasmic protein synthesis prevented induction of all aspects of cellular senescence in normal and tumor-derived human cells. It allowed the cells to continuously grow with no sign of senescent features in the presence of various inducers. It also delayed replicative senescence in normal human fibroblasts. Moreover, it allowed for growth of the cells that had entered a senescent state. When adult worms of the nematode C. elegans were grown under protein-restricted conditions, their average and maximal lifespans were significantly extended. These results suggest that accumulation of cytoplasmic proteins due to imbalance in macromolecule synthesis is a fundamental cause of cellular senescence.
在多种细胞类型中，用适当的衰老诱导剂处理细胞可诱导细胞衰老或其等效现象。对细胞质蛋白质合成进行轻度限制可阻止正常和肿瘤来源的人类细胞中细胞衰老各方面的诱导。在存在各种诱导剂的情况下，它使细胞能够持续生长，没有衰老特征的迹象。它还延迟了正常人成纤维细胞的复制性衰老。此外，它允许已进入衰老状态的细胞生长。当线虫秀丽隐杆线虫的成虫在蛋白质限制条件下生长时，它们的平均寿命和最大寿命显著延长。这些结果表明，由于大分子合成失衡导致的细胞质蛋白质积累是细胞衰老的根本原因。
