The role of FGF2 in stress-induced cFos expression

Yifan Zhang
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Abstract

During periods of stress, organisms endocrine systems respond by releasing glucocorticoids which later get expressed through corticosterone, simplified as CORT. CORT is proved to express FGF2, proteins found in critical glial cells named astrocytes. Increased FGF2 expression leads to higher rate of cell proliferation - including neurons. Theres been discoveries that newborn neurons, specifically those who have been exposed to FGF2, led to early neuron activation and enhanced neuronal function. Whats unclear is whether FGF2 played a role in somehow newborn neurons having enhanced function and activating earlier than usual (by releasing the early activation gene cFos). An experiment has been outlined in order to test the hypothesis that FGF2 does indeed play a role in altering some neurons. Using nanoparticles containing the micro RNA of NUDT6 - a gene that suppresses FGF2 expression - to target FGF2 in adult male Sprague-Dawley rats would directly test if FGF2 played a role in enhanced neuron activation.
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FGF2 在应激诱导的 cFos 表达中的作用
在压力时期,生物体的内分泌系统会释放糖皮质激素,随后通过皮质酮(简化为 CORT)表达出来。CORT 被证明能表达 FGF2,这是一种在名为星形胶质细胞的关键神经胶质细胞中发现的蛋白质。FGF2 表达的增加会导致包括神经元在内的细胞增殖速度加快。研究发现,新生神经元,特别是那些暴露于 FGF2 的新生神经元,会导致早期神经元活化并增强神经元功能。目前还不清楚的是,FGF2 是否在某种程度上增强了新生神经元的功能并使其比平常更早激活(通过释放早期激活基因 cFos)。为了验证 FGF2 确实在改变某些神经元方面发挥作用的假设,我们概述了一项实验。使用含有抑制 FGF2 表达基因 NUDT6 的微 RNA 的纳米粒子来靶向成年雄性 Sprague-Dawley 大鼠体内的 FGF2,可以直接测试 FGF2 是否在增强神经元活化中发挥作用。
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