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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Upregulation of dihydropyrimidinase-related protein 2, spectrin alpha II chain, heat shock cognate protein 70 pseudogene 1 and tropomodulin 2 after focal cerebral ischemia in rats--a proteomics approach.
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Upregulation of dihydropyrimidinase-related protein 2, spectrin alpha II chain, heat shock cognate protein 70 pseudogene 1 and tropomodulin 2 after focal cerebral ischemia in rats--a proteomics approach.

机译：大鼠局灶性脑缺血后二氢嘧啶酶相关蛋白2，血影蛋白αII链，热休克同源蛋白70假基因1和原调节蛋白2的上调-一种蛋白质组学方法。

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In recent years, there are an increasing number of proteomics studies that investigated the alterations in the protein expression relevant to human diseases but none for stroke. We, therefore, attempted such a study in a paradigm of focal cerebral ischemia in rat. Rats were subjected to cerebral ischemia by unilateral occlusion of the middle cerebral artery. Global protein analysis was performed after 24h on the lesioned and sham-control cerebral cortex using two-dimensional gel electrophoresis. Protein spots with more than a 3-fold change in intensity were identified by mass spectrometry. Middle cerebral artery occlusion (MCAO) caused infarct volume of 18-22% predominantly in the cortex of the lesioned hemisphere. Two-dimensional gel electrophoresis resolved about 1500 protein spots of which only 12 were significantly upregulated by 3-46-fold. Three spots were identified to be dihydropyrimidinase-related protein 2 (DRP-2, also known as collapsin response mediator protein 2 (CRMP-2) or turned on after division, 64 kD protein (TOAD-64)). The spots varied in pI values only and this may reflect different phosphorylation status of the same protein. Two spots were identified as spectrin alpha II chain (rat fragment, also known as alpha-fodrin or non-erythroid alpha chain, SPNA-2); and one spot each for heat shock cognate protein 70 pseudogene 1 (HSC70-ps1, also known as heat shock protein 8 pseudogene 1), and tropomodulin 2 (Tmod2). The upregulation of protein expression was corroborated by observed upregulation of mRNA expression. The remaining five spots were not identified satisfactorily. As DRP-2, spectrin, and Tmod2 are involved in axonal and neurite growth as well as synaptic plasticity and maturation, the presently observed upregulation of the expression of these proteins may indicate active neuroregeneration and repair at 24h after the induction of cerebral ischemia.
机译：近年来，越来越多的蛋白质组学研究调查了与人类疾病相关的蛋白质表达的变化，但对于中风却没有。因此，我们尝试在大鼠局灶性脑缺血范例中进行此类研究。通过单侧阻塞大脑中动脉对大鼠进行脑缺血。 24小时后，使用二维凝胶电泳对病变和假对照大脑皮层进行全局蛋白分析。通过质谱鉴定强度变化超过3倍的蛋白质斑点。大脑中动脉闭塞（MCAO）导致梗死面积占病变半球皮层的18-22％。二维凝胶电泳解析了约1500个蛋白斑点，其中只有12个被显着上调了3-46倍。三个斑点被确定为二氢嘧啶酶相关蛋白2（DRP-2，也称为胶原蛋白应答介导蛋白2（CRMP-2）或分裂后打开的64 kD蛋白（TOAD-64））。这些斑点的pI值仅变化，这可能反映了同一蛋白质的不同磷酸化状态。将两个斑点鉴定为血影蛋白αII链（大鼠片段，也称为α-fodrin或非红系α链，SPNA-2）;一个点分别为热休克同源蛋白70假基因1（HSC70-ps1，也称为热激蛋白8假基因1）和原代调节蛋白2（Tmod2）。通过观察到mRNA表达的上调来证实蛋白质表达的上调。其余五个斑点未令人满意地鉴定。由于DRP-2，血影蛋白和Tmod2参与轴突和神经突的生长以及突触可塑性和成熟，因此，目前观察到的这些蛋白表达的上调可能表明在脑缺血后24h内活跃的神经再生和修复。

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