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基因表达谱分析甲基强的松龙体外抑制神经祖细胞增殖的作用。

Analysis of methylprednisolone-induced inhibition on the proliferation of neural progenitor cells in vitro by gene expression profiling.

机构信息

Department of Orthopedics of Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Yanjiangxi Road 107, 510120 Guangzhou, China.

出版信息

Neurosci Lett. 2012 Sep 27;526(2):154-9. doi: 10.1016/j.neulet.2012.07.047. Epub 2012 Aug 2.

Abstract

Recently, it has been proved that methylprednisolone has inhibition effect on the proliferation of endogenous neural progenitor cells (NPCs) after spinal cord injury (SCI). Similar effect has also been found on NPCs cultured in vitro. However, the mechanism remains to be fully delineated. The purpose of this study is to investigate the potential molecular mechanism of this effect in NPCs cultured in vitro by gene expression profiling. Fetal mouse brain-derived NPCs were divided into 2 groups: NPCs incubated with methylprednisolone as a model of the methylprednisolone treatment after SCI, and without methylprednisolone as the control group. After the cell quantitative analysis and CCK-8 assay, the microarray analysis was carried out. Genes differentially expressed between NPCs treated with and without methylprednisolone were extracted. It was observed that the expression of 143 genes, including many members of distinct families, such as hypoxia inducible factors and neurotransmitter receptors, were significantly changed in response to the methylprednisolone treatment. Our results provide global molecular insights into the mechanisms of methylprednisolone-induced proliferation inhibition effect and suggest that EdnrB may play an important role in this effect.

摘要

最近已经证实,甲泼尼龙对脊髓损伤(SCI)后内源性神经祖细胞(NPC)的增殖具有抑制作用。在体外培养的 NPC 中也发现了类似的作用。然而,其机制仍有待充分描述。本研究旨在通过基因表达谱分析,探讨体外培养的 NPC 中这种作用的潜在分子机制。将胎鼠脑源性 NPC 分为 2 组:用甲泼尼龙孵育的 NPC 作为 SCI 后甲泼尼龙治疗的模型组,无甲泼尼龙孵育的 NPC 作为对照组。进行细胞定量分析和 CCK-8 检测后,进行了微阵列分析。提取了 NPC 中处理组和对照组之间差异表达的基因。结果观察到 143 个基因的表达发生了显著变化,包括缺氧诱导因子和神经递质受体等不同家族的许多成员。这些结果为甲泼尼龙诱导的增殖抑制作用的机制提供了全面的分子见解,并表明 EdnrB 可能在该作用中发挥重要作用。

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