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猪大脑皮质提取物诱导性脑出血后的蛋白质组学分析。

Proteomic Analysis of Cerebral Cortex Extracts from Sus scrofa with Induced Hemorrhagic Stroke.

机构信息

Research Institute of General Pathology and Pathophysiology, Moscow, Russia.

V.N. Orehovich Institute of Biomedical Chemistry, 10, Pogodinskaya st, Moscow, Russian Federation, 119121.

出版信息

J Mol Neurosci. 2018 May;65(1):28-34. doi: 10.1007/s12031-018-1064-8. Epub 2018 Apr 26.

DOI:10.1007/s12031-018-1064-8
PMID:29700768
Abstract

Cerebrovascular diseases, including stroke and micro stroke, are the main causes of death in contemporary society. Hemorrhagic stroke is the fast emerging defficiency in the brain function resulting from disturbance of blood supply to the brain caused by the rapture of blood vessels (Lopez et al. in Proteomics Clin Appl 6:190-200, 2012). The influence of a model hemorrhagic stroke on white pigs with the change in the protein profile of their cortical samples 24 h and 2 months after the stroke was examined using mass-spectrometric analysis. Different proteins (n = 30) were identified, and their content was elevated. These proteins are involved in the mechanisms of neuroprotection, including compensation of oxidative stress (TXN, SNCA, PRDX6, ENO1), prevention of unwanted protein aggregation and apoptosis (PTMA, SNCA, SNCB), release of neurotransmitters (GAPDH, PEBP1) and assembly of the cytoskeleton (ACTA2, PTMA, TUBA4A, TUBA1D), etc. Also, a group of seven Ras family proteins involved in the regulation of cell proliferation and differentiation was found in the samples taken 24 h following the stroke. The relative concentrations of most of the proteins in the samples taken 2 months after the stroke demonstrate intermediate values between the control sample and the sample taken in 24 h, indicating the extinction of change in the protein profile with time. During the first 24 h after the stroke, there is an increase in protein fractions participating in exocytosis, synaptic plasticity/signaling, and support of neurotransmitter transport. Such shift in the weight of protein functional clusters can be attributed to activation of compensatory mechanisms in the body focused on neuroprotection.

摘要

脑血管疾病,包括中风和微中风,是当代社会死亡的主要原因。出血性中风是由于血管破裂导致大脑供血中断而迅速出现的大脑功能丧失(Lopez 等人,《蛋白质组学临床应用》6:190-200, 2012)。使用质谱分析检查了模型出血性中风对 24 小时和中风后 2 个月皮质样本中白猪的影响,观察到蛋白质图谱的变化。鉴定了不同的蛋白质(n=30),其含量升高。这些蛋白质参与神经保护机制,包括氧化应激的补偿(TXN、SNCA、PRDX6、ENO1)、防止不必要的蛋白质聚集和细胞凋亡(PTMA、SNCA、SNCB)、神经递质的释放(GAPDH、PEBP1)和细胞骨架的组装(ACTA2、PTMA、TUBA4A、TUBA1D)等。此外,在中风后 24 小时采集的样本中还发现了一组参与细胞增殖和分化调节的七个 Ras 家族蛋白。中风后 2 个月采集的样本中大多数蛋白质的相对浓度介于对照样本和中风后 24 小时采集的样本之间,表明随着时间的推移,蛋白质图谱的变化逐渐消失。在中风后的前 24 小时内,参与胞吐作用、突触可塑性/信号转导和神经递质转运支持的蛋白质分数增加。这种蛋白质功能簇的权重变化可能归因于身体激活了以神经保护为重点的补偿机制。

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