Transcriptional regulation of ES cell by FGF signalling [RN18147]

FGF4 paracrine signaling through FGF receptors is believed to induce Erk activity and promotes the exit from pluripotency. However, we have recently observed that FGF4 and FGF2 have opposing effects on mES cell fate. The aim of this study was to understand the underlying transcriptional changes associated with these opposing actions. Overall design: Mouse embryonic stem cells were grown in a naïve state of pluripotency using 2iLIF media and subsequently stimulated with FGF2 in N2B27 media for 0hrs, 15min, 1hrs, 24hrs and 48hrs.

普遍认为，经由成纤维细胞生长因子受体（FGF receptors）介导的成纤维细胞生长因子4（FGF4）旁分泌信号通路可激活细胞外调节蛋白激酶（Erk）的活性，并促进细胞退出多能状态。然而，我们近期的研究发现，FGF4与FGF2对小鼠胚胎干细胞（mES cell）的细胞命运具有相反的调控作用。本研究旨在阐明与这些相反调控作用相关的潜在转录变化。
实验整体设计：采用2iLIF培养基培养小鼠胚胎干细胞，使其维持在多能性幼稚态，随后将细胞置于N2B27培养基中，用FGF2分别刺激0小时、15分钟、1小时、24小时及48小时。