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抑制糖原合酶激酶-3 可增强成年人类嗅上皮神经前体细胞的分化,减少其增殖。

Inhibition of glycogen synthase kinase-3 enhances the differentiation and reduces the proliferation of adult human olfactory epithelium neural precursors.

机构信息

Institute of Biomaterials and Biomedical Engineering, University of Toronto, Toronto, Ontario, Canada.

出版信息

Exp Cell Res. 2011 Sep 10;317(15):2086-98. doi: 10.1016/j.yexcr.2011.06.004. Epub 2011 Jun 25.

Abstract

The olfactory epithelium (OE) contains neural precursor cells which can be easily harvested from a minimally invasive nasal biopsy, making them a valuable cell source to study human neural cell lineages in health and disease. Glycogen synthase kinase-3 (GSK-3) has been implicated in the etiology and treatment of neuropsychiatric disorders and also in the regulation of murine neural precursor cell fate in vitro and in vivo. In this study, we examined the impact of decreased GSK-3 activity on the fate of adult human OE neural precursors in vitro. GSK-3 inhibition was achieved using ATP-competitive (6-bromoindirubin-3'-oxime and CHIR99021) or substrate-competitive (TAT-eIF2B) inhibitors to eliminate potential confounding effects on cell fate due to off-target kinase inhibition. GSK-3 inhibitors decreased the number of neural precursor cells in OE cell cultures through a reduction in proliferation. Decreased proliferation was not associated with a reduction in cell survival but was accompanied by a reduction in nestin expression and a substantial increase in the expression of the neuronal differentiation markers MAP1B and neurofilament (NF-M) after 10 days in culture. Taken together, these results suggest that GSK-3 inhibition promotes the early stages of neuronal differentiation in cultures of adult human neural precursors and provide insights into the mechanisms by which alterations in GSK-3 signaling affect adult human neurogenesis, a cellular process strongly suspected to play a role in the etiology of neuropsychiatric disorders.

摘要

嗅上皮(OE)包含神经前体细胞,这些细胞可以很容易地从微创性鼻活检中获得,这使得它们成为研究人类神经细胞谱系在健康和疾病中的宝贵细胞来源。糖原合酶激酶-3(GSK-3)已被牵连到神经精神疾病的病因和治疗中,也被牵连到体外和体内调节鼠神经前体细胞命运。在这项研究中,我们研究了降低 GSK-3 活性对体外成人 OE 神经前体细胞命运的影响。通过使用 ATP 竞争性(6-溴靛红-3'-肟和 CHIR99021)或底物竞争性(TAT-eIF2B)抑制剂来抑制 GSK-3,以消除由于脱靶激酶抑制对细胞命运的潜在混杂影响。GSK-3 抑制剂通过减少增殖来减少 OE 细胞培养物中的神经前体细胞数量。增殖减少与细胞存活减少无关,但伴随着巢蛋白表达减少和 MAP1B 和神经丝(NF-M)的神经元分化标志物的表达显著增加,在培养 10 天后。总之,这些结果表明,GSK-3 抑制促进了成人神经前体细胞培养物中神经元分化的早期阶段,并深入了解了 GSK-3 信号转导改变如何影响成人神经发生的机制,这一细胞过程强烈怀疑在神经精神疾病的病因中发挥作用。

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