Bmal1-deficient mouse fibroblast cells do not provide premature cellular senescence in vitro
Bmal1-deficient mouse fibroblast cells do not provide premature cellular senescence in vitro
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DOI：
10.1080/07420528.2018.1430038
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发表时间：
2018-01
影响因子：
2.8
通讯作者：
Yasukazu Nakahata;Shiori Yasukawa;F. D. Khaidizar;S. Shimba;Takaaki Matsui;Yasumasa Bessho
中科院分区：
文献类型：
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作者：
Yasukazu Nakahata;Shiori Yasukawa;F. D. Khaidizar;S. Shimba;Takaaki Matsui;Yasumasa Bessho
Bmal 1基因是生物钟的核心基因。Bmal 1 −/−小鼠表现出生物钟的破坏和寿命短的过早衰老表型。然而，很少有人知道Bmal 1的破坏是否会导致细胞水平的过早衰老。在这里，我们建立了来自Bmal 1 −/−小鼠的原代小鼠胚胎成纤维细胞（MEF），并研究了其对细胞衰老的影响。出乎意料的是，显示昼夜节律振荡中断的Bmal 1 −/−初级MEFs既没有经历过早的复制也没有经历应激诱导的细胞衰老。因此，我们的研究结果揭示，Bmal 1是不需要在体外细胞衰老，表明生物钟不控制在体外细胞衰老。
ABSTRACT Bmal1 is a core circadian clock gene. Bmal1−/− mice show disruption of the clock and premature aging phenotypes with a short lifespan. However, little is known whether disruption of Bmal1 leads to premature aging at cellular level. Here, we established primary mouse embryonic fibroblast (MEF) cells derived from Bmal1−/− mice and investigated its effects on cellular senescence. Unexpectedly, Bmal1−/− primary MEFs that showed disrupted circadian oscillation underwent neither premature replicative nor stress-induced cellular senescence. Our results therefore uncover that Bmal1 is not required for in vitro cellular senescence, suggesting that circadian clock does not control in vitro cellular senescence.