Glia:NF-Y调控网络调节少突胶质细胞中谷氨酸受体4的表达

2018-05-11 cuiguizong MedSci原创

英国伯明翰大学医学和牙科学院的神经科学与眼科研究组的Begum G近日在Glia发表了一篇文章,他们发现,CCAAT结合转录因子NF-Yb是Gria4(GluA4基因)的新型转录调节因子,并且是少突胶质细胞中兴奋性毒性死亡的关键调控因子。

英国伯明翰大学医学和牙科学院的神经科学与眼科研究组的Begum G近日在Glia发表了一篇文章,他们发现,CCAAT结合转录因子NF-Yb是Gria4(GluA4基因)的新型转录调节因子,并且是少突胶质细胞中兴奋性毒性死亡的关键调控因子。

对兴奋性毒性敏感的神经细胞高度表达谷氨酸受体亚基4(GluA4)。少突胶质细胞前体细胞(OPC)在缺氧缺血性损伤的关键时期表达水平较高。因此,研究兴奋性GluA4激活的下游转录网络对干预治疗是有希望的。

他们发现,Gria4包含CCAAT序列的区域是一个新调控区域,与NF-Yb的结合受兴奋性因子的调节。NF-Yb结合引起的兴奋性改变与Gria4转录水平改变相关,而敲低NF-Yb的水平可以导致含有该调节区域转录水平的变化。永生化和原代OPC细胞实验数据揭示,通过RNAi的方法和使用NF-Yb药理学破坏,都可以改变Gria4的转录水平。NF-Yb药物可以诱导细胞凋亡并影响一组凋亡基因的表达。

这些数据首次揭示了调控Gria4的反式作用机制,并指出NF-Yb调控网络是促进少突胶质细胞前体细胞存活的药理学潜在靶点。

原文出处:

Begum, G., et al., NF-Y-dependent regulation of glutamate receptor 4 expression and cell survival in cells of the oligodendrocyte lineage. Glia, 2018.

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