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生物钟基因通过Wnt信号通路促进3T3-L1细胞增殖。

CLOCK promotes 3T3-L1 cell proliferation via Wnt signaling.

作者信息

Zhu Zhu, Hua Bingxuan, Xu Lirong, Yuan Gongsheng, Li Ermin, Li Xiaobo, Sun Ning, Yan Zuoqin, Lu Chao, Qian Ruizhe

机构信息

Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Fudan University, Shanghai, China.

Department of Orthopedics, Zhongshan Hospital, Fudan University, Shanghai, China.

出版信息

IUBMB Life. 2016 Jul;68(7):557-68. doi: 10.1002/iub.1512. Epub 2016 May 18.

Abstract

Circadian genes control most of the physiological functions including cell cycle. Cell proliferation is a critical factor in the differentiation of progenitor cells. However, the role of Clock gene in the regulation of cell cycle via wingless-type (Wnt) pathway and the relationship between Clock and adipogenesis are unclear. We found that the circadian locomotor output cycles kaput (Clock) regulated the proliferation and the adipogenesis of 3T3-L1 preadipocytes. We found that Clock attenuation inhibited the viability of 3T3-L1 preadipocytes in the cell counting kit 8. The expression of c-Myc and Cyclin D1 decreased dramatically in 3T3-L1 when Clock was silenced with short interfering RNA and was also decreased in fat tissue and adipose tissue-derived stem cells of Clock(Δ19) mice. Clock directly controls the expression of the components of Wnt signal transduction pathway, which was verified by serum shock, chromatin immunoprecipitation, Western blot, and quantitative real-time polymerase chain reaction (qRT-PCR). Furthermore, IWR-1, a Wnt signal pathway inhibitor, inhibited the cell cycle promotion by CLOCK, which was detected by cell viability assay, flow cytometry, and qRT-PCR. Therefore, CLOCK transcription control of Wnt signaling promotes cell cycle progression in 3T3-L1 preadipocytes. Clock inhibited the adipogenesis on day 2 in 3T3-L1 cells via Oil Red O staining and qRT-PCR detection and probably related to cellular differentiation. These data provide evidence that the circadian gene Clock regulates the proliferation of preadipocytes and affects adipogenesis. © 2016 IUBMB Life, 68(7):557-568, 2016.

摘要

昼夜节律基因控制着包括细胞周期在内的大多数生理功能。细胞增殖是祖细胞分化的关键因素。然而,生物钟基因通过无翅型(Wnt)信号通路调控细胞周期的作用以及生物钟与脂肪生成之间的关系尚不清楚。我们发现昼夜节律运动输出周期基因(Clock)调节3T3-L1前脂肪细胞的增殖和脂肪生成。我们发现,在细胞计数试剂盒8检测中,Clock基因表达减弱会抑制3T3-L1前脂肪细胞的活力。当用短发夹RNA沉默Clock基因时,3T3-L1细胞中c-Myc和细胞周期蛋白D1的表达显著下降,在Clock(Δ19)小鼠的脂肪组织和脂肪组织来源的干细胞中也下降。Clock直接控制Wnt信号转导通路成分的表达,这通过血清休克、染色质免疫沉淀、蛋白质免疫印迹和定量实时聚合酶链反应(qRT-PCR)得到验证。此外,Wnt信号通路抑制剂IWR-1抑制了CLOCK对细胞周期的促进作用,这通过细胞活力测定、流式细胞术和qRT-PCR检测到。因此,CLOCK对Wnt信号的转录调控促进了3T3-L1前脂肪细胞的细胞周期进程。通过油红O染色和qRT-PCR检测发现,Clock在第2天抑制3T3-L1细胞的脂肪生成,这可能与细胞分化有关。这些数据证明,昼夜节律基因Clock调节前脂肪细胞的增殖并影响脂肪生成。©2016国际生物化学与分子生物学联盟生命科学部,68(7):557 - 568,2016年。

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