Yuan Yanyan, Xi Yang, Chen Jiayi, Zhu Pan, Kang Jinyu, Zou Zuquan, Wang Fuyan, Bu Shizhong
Runliang Diabetes Laboratory, Diabetes Research Center, Zhejiang Provincial Key Laboratory of Pathophysiology, School of Medicine, Ningbo University, Ningbo, 315211, China.
Biochem Biophys Res Commun. 2017 Jan 22;482(4):1360-1366. doi: 10.1016/j.bbrc.2016.12.042. Epub 2016 Dec 9.
Signal transducer and activator of transcription 3 (STAT3) is abundantly expressed in the adipose tissue of obese mice and humans, but the role of STAT3 in adipogenesis is still not fully understood. In the present study, we discovered an activation of STAT3 during the early differentiation stage of mouse 3T3-L1 preadipocytes. Stat3 knockdown using siRNA blocked cell cycle progression of both preadipoctes and early differentiating cells. Moreover, accumulation of lipid droplets was inhibited by Stat3 knockdown. Importantly, in the nucleus of early differentiating cells, we demonstrated that STAT3 protein co-localized with high-mobility-group protein AT-hook 2 (HMGA2), which was reported to promote adipogenesis in a previous study. Taken together, our data indicate that STAT3 and HMGA2 cooperatively promote adipogenesis which highlight a more detail understanding of STAT3 related transcription factor network during adipogenesis.
信号转导与转录激活因子3(STAT3)在肥胖小鼠和人类的脂肪组织中大量表达,但STAT3在脂肪生成中的作用仍未完全明确。在本研究中,我们发现在小鼠3T3-L1前脂肪细胞的早期分化阶段STAT3被激活。使用小干扰RNA敲低Stat3可阻断前脂肪细胞和早期分化细胞的细胞周期进程。此外,敲低Stat3可抑制脂滴的积累。重要的是,在早期分化细胞的细胞核中,我们证实STAT3蛋白与高迁移率族蛋白AT钩2(HMGA2)共定位,先前的一项研究报道HMGA2可促进脂肪生成。综上所述,我们的数据表明STAT3和HMGA2协同促进脂肪生成,这为深入了解脂肪生成过程中与STAT3相关的转录因子网络提供了更多细节。