Differential regulation of ciliary neurotrophic factor (CNTF) and CNTF receptor alpha (CNTFR alpha) expression following focal cerebral ischemia.
Differential regulation of ciliary neurotrophic factor (CNTF) and CNTF receptor alpha (CNTFR alpha) expression following focal cerebral ischemia.
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局灶性脑缺血后睫状神经营养因子（CNTF）和CNTF受体α（CNTFRα）表达的差异调节。
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发表时间：
1998
期刊：
影响因子：
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通讯作者：
J. Kuo
中科院分区：
文献类型：
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作者：
T. Lin;P. Wang;S. Chi;J. Kuo
睫状神经营养因子（CNTF）是细胞因子的一员，对睫状神经元、运动交感神经元、感觉神经元、视网膜神经元和海马神经元具有营养作用。在本研究中，我们研究了CNTF和CNTF受体α（CNTFR α）mRNA的时间和空间表达谱的局灶性脑缺血模型引起的短暂闭塞的右侧大脑中动脉和两个颈总动脉。北方印迹分析表明，在1.2 kb的CNTF mRNA转录在大鼠缺血皮层的短暂缺血60分钟的伤害缓慢和持续增加。在大鼠缺血60 min再灌注72 h后，观察到缺血皮质中CNTFR α mRNA的2.1 kb转录物延迟减少。原位杂交研究显示，在大脑中的大多数神经元中的CNTFR α mRNA的组成性表达。再灌注4小时后，在同侧齿状回观察到CNTFR α mRNA表达增加，这与缺血皮质中的下调相反。再灌注1天后，在梗死区域内，皮质层II中CNTFR α mRNA显著增加，但皮质层V中CNTFR α mRNA减少。再灌注3天后，在梗死区域内未检测到CNTFR α mRNA的信号。再灌注1周后，尽管在观察到反应性星形胶质细胞的坏死区域周围区域中的CNTFR α mRNA水平未观察到显著变化，但观察到CNTF mRNA信号显著增加。总之，CNTF和CNTFR α mRNA的差异调节在缺血皮质中被注意到。CNTF受体表达的区域差异，缺血皮质和同侧齿状回之间，以及皮质层II和V之间的梗死区域。CNTF mRNA，而不是CNTFR α mRNA，有一个显着的增加，在该地区直接相邻的坏死。这些差异调节的机制和病理生理意义仍有待研究。
Ciliary neurotrophic factor (CNTF) is a member of cytokines, with trophic effects on ciliary, motor sympathetic, sensory, retinal and hippocampal neurons. In the present study, we examined the temporal and spatial expression profiles of CNTF and CNTF receptor alpha (CNTFR alpha) mRNAs in a focal cerebral ischemia model induced by transient occlusion of the right middle cerebral artery and both common carotid arteries. Northern blot analysis showed a slow and sustained increase in the 1.2 kb transcript of CNTF mRNA in the ischemic cortex of rats subjected to a transient 60 min ischemic insult. A delayed decrease in the 2.1 kb transcript of CNTFR alpha mRNA in the ischemic cortex was observed in rats subjected to 60 min ischemia followed by 72 h of reperfusion. In situ hybridization studies revealed constitutive expression of CNTFR alpha mRNA in the majority of neurons in the brain. Following 4 h of reperfusion, increased expression of CNTFR alpha mRNA was observed in the ipsilateral dentate gyrus, which is opposite to the down-regulation noted in the ischemic cortex. Within the infarct area CNTFR alpha mRNA had a marked increase in cortical layer II but a decrease in cortical layer V following 1 day of reperfusion. No signal of CNTFR alpha mRNA was detected within the infarct region following 3 days of reperfusion. Following 1 week of reperfusion, although no marked changes was observed in the level of CNTFR alpha mRNA in the area immediately surrounding the necrosis region where the reactive astrocytes were noted, a striking increase in the CNTF mRNA signal was noted. In summary, differential regulation of CNTF and CNTFR alpha mRNAs was noted in the ischemic cortex. Regional differences in CNTF receptor expression were noted between the ischemic cortex and ipsilateral dentate gyrus as well as between cortical layer II and V within the infarct region. CNTF mRNA, but not CNTFR alpha mRNA, had a marked increase in the area immediately adjacent to the necrosis. The mechanisms and patho-physiological significance for these differential regulation remain to be studied.