Involvement of IL‐1 family proteins in p38 linked cellular senescence of mouse embryonic fibroblasts
Involvement of IL‐1 family proteins in p38 linked cellular senescence of mouse embryonic fibroblasts
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DOI：
10.1016/j.febslet.2004.08.033
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发表时间：
2004-09
期刊：
影响因子：
3.5
通讯作者：
N. Uekawa;A. Nishikimi;K. Isobe;Y. Iwakura;M. Maruyama
中科院分区：
文献类型：
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作者：
N. Uekawa;A. Nishikimi;K. Isobe;Y. Iwakura;M. Maruyama
哺乳动物培养细胞的衰老本质上是由各种细胞外刺激引起的细胞分裂和细胞应激机制组织的。在此，我们发现，在体外培养的小鼠胚胎成纤维细胞(MEF)中，炎症细胞因子IL-1β(IL-1β)及其拮抗剂IL-1受体拮抗剂(IL-1ra)的表达受到衰老的诱导。在MEFS培养过程中，IL-1β表达的动力学与p38的激活动力学相似。我们还发现，在IL-1ra缺乏的MEF培养中，细胞生长明显加速衰老。我们的结果提示，IL-1β信号通路参与了p38相关细胞衰老的激活。
Senescence of mammalian cultured cells is essentially organized by a machinery of cell division and cellular stresses induced by various extracellular stimuli. Here, we show that in mouse embryonic fibroblasts (MEFs) culture in vitro, expression of an inflammatory cytokine, interleukin-1β (IL-1β) and its antagonist, IL-1 receptor antagonist (IL-1Ra) are induced by senescence. The kinetics of IL-1β-expression was similar to that of p38 activation during MEFs culture. We also found a distinguishable accelerated senescence in cell growth in IL-1Ra deficient MEFs culture. Our results suggest that IL-1β signaling pathway is involved in activation of p38 linked cellular senescence.