Dynamic Expression Pattern of Neuro-oncological Ventral Antigen 1 (Nova1) in the Rat Brain after Focal Cerebral Ischemia/Reperfusion Insults

Dynamic Expression Pattern of Neuro-oncological Ventral Antigen 1 (Nova1) in the Rat Brain after Focal Cerebral Ischemia/Reperfusion Insults
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局灶性脑缺血/再灌注损伤后大鼠脑中神经肿瘤腹侧抗原 1 (Nova1) 的动态表达模式

DOI:
10.1369/0022155412461255
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发表时间:
2013-01-01
影响因子:
3.2
通讯作者:
Zhang, Chenggang
Zhang, Chenggang
中科院分区:
生物学3区
文献类型:
--
作者:
Li, Hualing;Sun, Changqing;Zhang, Chenggang

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本研究旨在通过免疫组织化学评估神经肿瘤腹侧抗原 1 (Nova1) 在脑缺血/再灌注 (I/R) 损伤中的表达。 Sprague-Dawley (SD) 大鼠通过右大脑中动脉闭塞 (MCAO) 120 分钟,然后再灌注 1 天、7 天和 14 天来诱导局灶性脑 I/R 模型。结果显示,Nova1几乎在整个大脑中表达,但在海马、下丘脑、扣带皮层和内侧缰核中表达密度较高。再灌注1天后,Nova1神经元的免疫反应性显着增加,尤其是海马CA1区两侧。再灌注 1 天到 7 天之间,同侧 CA1 区域出现强烈反应。同样,在纹状皮层、齿状回和下丘脑的对侧观察到 Nova1 表达的强烈代偿反应。有趣的是,再灌注7天后,观察到更多的Nova1神经元易位到缺血侧下丘脑轴突的树突和生长锥。总之,我们的数据表明 Nova1 可能介导神经元反应性,并且其表达可能与大鼠大脑 I/R 损伤后的神经修复呈正相关。
The present study aimed to evaluate the expression of neuro-oncological ventral antigen 1 (Nova1) in cerebral ischemia/reperfusion (I/R) insults by immunohistochemistry. The focal cerebral I/R model was induced by right middle cerebral artery occlusion (MCAO) for 120 min followed by 1 day, 7 days, and 14 days of reperfusion in Sprague-Dawley (SD) rats. The results showed that Nova1 was expressed in nearly the whole brain, although with higher density in hippocampus, hypothalamus, cingulate cortex, and medial habenular nucleus. The immunoreactivity of Nova1 neurons was increased dramatically, especially on both sides of the hippocampal CA1 region, after 1 day of reperfusion. A strong response occurred at the ipsilateral CA1 region between 1 day and 7 days of reperfusion. Likewise, strong compensatory responses of Nova1 expression were observed on the contralateral side of the striate cortex, dentate gyrus, and hypothalamus. Interestingly, more Nova1 neurons were observed to translocate to the dendrites and growth cones of the axons in the hypothalamus on the ischemic side after 7 days of reperfusion. In conclusion, our data suggest that Nova1 might mediate neuronal responsiveness, and its expression might positively correlate with neural repair after I/R insults in the rat brain.