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首页> 外文期刊>Journal of Cellular Physiology >Activin-SMAD signaling is required for maintenance of porcine iPS cell self-renewal through upregulation of NANOG and OCT4 expression
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Activin-SMAD signaling is required for maintenance of porcine iPS cell self-renewal through upregulation of NANOG and OCT4 expression

机译：Activin-SMAD信号需要维护猪“诱导多能性”细胞的自我更新upregulation NANOG和OCT4表达式

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摘要

Porcine induced pluripotent stem cells (piPSCs) retain the enormous potential for farm animal reproduction and translational medicine, and have been reported by many laboratories worldwide. Some piPSC lines were bFGF-dependence and showed mouse EpiSC-like morphology; other lines were LIF-dependence and showed mouse ESC-like morphology. Metastable state of piPSC line that required both LIF and bFGF was also reported. Because bona fide pig embryonic stem cells were not available, uncovering piPSC state-specific regulatory circuitries was the most important task. In this study, we explored the function of Activin-SMAD signaling pathway and its downstream activated target genes in piPSCs. Transcriptome analysis showed that genes involved in Activin-SMAD signaling pathway were evidently activated during porcine somatic cell reprogramming, regardless piPSCs were LIF- or bFGF-dependent. Addition of Activin A and overexpression of SMAD2/3 significantly promoted expressions of porcine NANOG and OCT4, whereas inhibition of Activin-SMAD signaling by SB431542 and SMAD7 reduced NANOG and OCT4 expressions, and induced piPSCs differentiation exiting from pluripotent state. Our data demonstrate that activation of Activin-SMAD signaling pathway by addition of Activin A in culture medium is necessary for maintenance of self-renewal in porcine pluripotent stem cells.
机译：猪诱导多能干细胞(piPSCs)保留农场动物的巨大潜力繁殖和转化医学被世界各地的实验室报告。一些piPSC线路bFGF-dependence和显示鼠标EpiSC-like形态;LIF-dependence并显示鼠标ESC-like形态。需要生活和bFGF也报道。因为真正的猪胚胎干细胞无法获取,揭露piPSC具体由各州完成监管电路是最重要的的任务。Activin-SMAD信号通路及其下游在piPSCs激活靶基因。分析表明,基因参与Activin-SMAD信号通路是明显的在猪体细胞激活重组,无论piPSCs生活——或者bFGF-dependent。过度的SMAD2/3显著提升表达猪NANOG和OCT4,而抑制Activin-SMAD SB431542信号和SMAD7减少NANOG OCT4表达式和诱导piPSCs分化退出多能性状态。Activin-SMAD信号通路的激活培养基中添加苯丙酸诺龙需要维护的自我更新猪多能干细胞。

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