An G, Lin T N, Liu J S, Hsu C Y
Division of Restorative Neurology, Baylor College of Medicine, Houston, TX 77030.
Biochem Biophys Res Commun. 1992 Nov 16;188(3):1104-10. doi: 10.1016/0006-291x(92)91345-q.
Krox-20 is one of the transcription factors of "zinc finger" family. The expression of Krox-20 was investigated in a rat focal cerebral ischemia model by Northern blot analysis and in situ hybridization. Northern blot analysis showed that ischemia for 30 min which caused little cortical infarction induced a 29-fold increase in Krox-20 mRNA signal exclusively in the ischemic cortex. Ischemia for 90 min which led to large cortical infarction induced Krox-20 mRNA not only in the ischemic cortex but also in the ipsilateral hippocampus. The induction of Krox-20 mRNA was rapid, transient and appeared to be controlled at the transcriptional level, as indicated by nuclear run-on assays. The regional induction of Krox-20 mRNA was further confirmed by in situ hybridization. These results suggest that the expression of transcription factor genes may play a role in the post-ischemic changes of the injured brain.
Krox-20是“锌指”家族的转录因子之一。通过Northern印迹分析和原位杂交技术，在大鼠局灶性脑缺血模型中研究了Krox-20的表达情况。Northern印迹分析显示，缺血30分钟仅在缺血皮层引起轻微皮质梗死，但导致Krox-20 mRNA信号增加了29倍。缺血90分钟导致大面积皮质梗死，不仅在缺血皮层诱导了Krox-20 mRNA表达，同侧海马也有表达。核转录分析表明，Krox-20 mRNA的诱导迅速、短暂，且似乎在转录水平受到调控。原位杂交进一步证实了Krox-20 mRNA的区域诱导现象。这些结果表明，转录因子基因的表达可能在损伤脑的缺血后变化中发挥作用。
