Proteome analysis of up-regulated proteins in the rat spinal cord induced by transection injury

Proteome analysis of up-regulated proteins in the rat spinal cord induced by transection injury
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DOI:
10.1002/pmic.200500296
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发表时间:
2006-01-01
期刊:
影响因子:
3.4
通讯作者:
Liu, SJ
Liu, SJ
中科院分区:
生物学3区
文献类型:
--
作者:
Ding, QX;Wu, Z;Liu, SJ

文献摘要

被引文献

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成年哺乳动物的中枢神经系统无法再生,这促使我们揭示与受损中枢神经系统相关的相关蛋白质。在本文中,对雄性成年大鼠进行胸椎椎板切除术(作为假手术对照)或胸椎脊髓横断术。手术后五天,将整个脊髓组织解剖并分成水溶性部分(溶解在 Tris 缓冲液中)和水不溶性部分(溶解在含有离液剂和表面活性剂的溶液中)用于 2-DE。通过MS进行蛋白质鉴定并通过Western blot进一步证实。结果,受损脊髓中超过 30 个蛋白点的表达上调不少于 1.5 倍。这些鉴定出的蛋白质可能在损伤和修复过程中发挥不同的作用,并且可以在功能上分为几个不同的组,例如应激反应和代谢变化、脂质和蛋白质变性、神经存活和再生。特别是,11-锌指蛋白和磷脂酰肌醇蛋白聚糖的过度表达可能是抑制轴突生长和再生的原因。此外,还发现三种具有新序列的未知蛋白质因脊髓损伤而上调。这些分子的进一步表征可能有助于我们更深入地了解成人中枢神经系统无法再生的机制。
The inability of the CNS to regenerate in adult mammals propels us to reveal associated proteins involved in the injured CNS. In this paper, either thoracic laminectomy (as sham control) or thoracic spinal cord transection was performed on male adult rats. Five days after surgery, the whole spinal cord tissue was dissected and fractionated into water-soluble (dissolved in Tris buffer) and water-insoluble (dissolved in a solution containing chaotropes and surfactants) portions for 2-DE. Protein identification was performed by MS and further confirmed by Western blot. As a result, over 30 protein spots in the injured spinal cord were shown to be up-regulated no less than 1.5-fold. These identified proteins possibly play various roles during the injury and repair process and may be functionally categorized as several different groups, such as stress-responsive and metabolic changes, lipid and protein degeneration, neural survival and regeneration. In particular, over-expression of 11-zinc finger protein and glypican may be responsible for the inhibition of axonal growth and regeneration. Moreover, three unknown proteins with novel sequences were found to be up-regulated by spinal cord injury. Further characterization of these molecules may help us come closer to understanding the mechanisms that underlie the inability of the adult CNS to regenerate.