Expression of damage-induced neuronal endopeptidase (DINE) mRNA in peri-infarct cortical and thalamic neurons following middle cerebral artery occlusion
Expression of damage-induced neuronal endopeptidase (DINE) mRNA in peri-infarct cortical and thalamic neurons following middle cerebral artery occlusion
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DOI：
10.1111/j.1471-4159.2004.02784.x
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发表时间：
2004-11-01
影响因子：
4.7
通讯作者：
Kiyama, H
中科院分区：
文献类型：
--
作者：
Ohba, N;Kiryu-Seo, S;Kiyama, H
损伤诱导的神经元内肽酶（DINE）是最近在周围神经损伤模型中发现的一种独特的神经损伤相关分子。本研究的目的是确定DINE在大脑中动脉（MCA）闭塞后的成年大鼠中的表达谱和分布。局灶性脑缺血诱导DINE mRNA在梗死灶周围皮质和丘脑特定核团的迟发性和延长性表达。使用免疫组织化学和原位杂交的双重标记显示，DINE mRNA仅在神经元标记物NeuN呈阳性的细胞中表达。以前建立的神经解剖纤维连接的知识表明，DINE mRNA表达的区域投射其轴突或通过梗死的核心区域。这种独特的表达谱与神经损伤神经元的标志物激活转录因子-3（ATF-3）的表达谱相似。98%以上的ATF-3阳性神经元同时表达DINE mRNA，表明DINE在CNS和PNS损伤神经元中均有表达。由于DINE表达促进抗氧化活性，我们的研究结果表明，DINE可能作为一种神经保护分子在缺血性损伤的神经元。
Damage-induced neuronal endopeptidase (DINE) is a unique nerve-injury associated molecule, which was recently identified in a peripheral nerve injury model. The aim of this study was to determine the expression profiles and distribution of DINE in adult rats after middle cerebral artery (MCA) occlusion. Focal cerebral ischemia induced late-onset and prolonged expression of DINE mRNA in the peri-infarct cortex and specific nuclei of thalamus. Double labeling using immunohistochemistry and in situ hybridization revealed that DINE mRNA was exclusively expressed in cells that were positive to a neuronal marker NeuN. Previously established knowledge on neuroanatomical fiber connection suggests that DINE mRNA was expressed in areas projecting their axons to or through the core region of the infarction. This unique expression profile was similar to that of activating transcription factor-3 (ATF-3), which is a marker of nerve-injured neuron. More than 98% of ATF-3 immunoreactive neurons simultaneously expressed DINE mRNA, suggesting that DINE expression is observed in injured neurons of CNS as well as PNS. Since DINE expression promotes antioxidant activity, our results suggest that DINE may act as a neuroprotective molecule in neurons under ischemic insult.