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SOD1 G93A小鼠脊髓和大脑中潜在重叠的差异表达蛋白的初步分析

Preliminary Analysis of Potentially Overlapping Differentially Expressed Proteins in Both the Spinal Cord and Brain of SOD1 G93A Mice.

作者信息

Jiang Shi-Shi, Nie Hong-Bing, Hua Shan, Xie Meng, Xu Ren-Shi

机构信息

Department of Neurology, Jiangxi Provincial People's Hospital, Clinical College of Nanchang Medical College, The First Affiliated Hospital of Nanchang Medical College, Nanchang, 330006, Jiangxi, China.

Department of Ultrasonography, Jiangxi Provincial People's Hospital, The First Affiliated Hospital of Nanchang Medical College, Nanchang, 330006, Jiangxi, China.

出版信息

Curr Protein Pept Sci. 2025;26(1):57-75. doi: 10.2174/0113892037293525240621120033.

DOI:10.2174/0113892037293525240621120033
PMID:38984582
Abstract

OBJECTIVE

Proteomic elucidation is an essential step in improving our understanding of the biological properties of proteins in amyotrophic lateral sclerosis (ALS).

METHODS

Preliminary proteomic analysis was performed on the spinal cord and brain of SOD1 G93A (TG) and wild-type (WT) mice using isobaric tags for relative and absolute quantitation.

RESULTS

Partial up- and downregulated proteins showing significant differences between TG and WT mice were identified, of which 105 proteins overlapped with differentially expressed proteins in both the spinal cord and brain of progression mice. Bioinformatic analyses using Gene Ontology, a cluster of orthologous groups, and Kyoto Encyclopedia of Genes and Genomes pathway revealed that the significantly up- and downregulated proteins represented multiple biological functions closely related to ALS, with 105 overlapping differentially expressed proteins in the spinal cord and brain at the progression stage of TG mice closely related to 122 pathways. Differentially expressed proteins involved in a set of molecular functions play essential roles in maintaining neural cell survival.

CONCLUSION

This study provides additional proteomic profiles of TG mice, including potential overlapping proteins in both the spinal cord and brain that participate in pathogenesis, as well as novel insights into the up- and downregulation of proteins involved in the pathogenesis of ALS.

摘要

目的

蛋白质组学解析是增进我们对肌萎缩侧索硬化症(ALS)中蛋白质生物学特性理解的关键步骤。

方法

使用相对和绝对定量的等压标签,对SOD1 G93A(转基因,TG)小鼠和野生型(WT)小鼠的脊髓和脑进行初步蛋白质组学分析。

结果

鉴定出了TG小鼠和WT小鼠之间部分上调和下调且存在显著差异的蛋白质,其中105种蛋白质与疾病进展期小鼠脊髓和脑中差异表达的蛋白质重叠。使用基因本体论、直系同源簇和京都基因与基因组百科全书通路进行的生物信息学分析表明,显著上调和下调的蛋白质代表了与ALS密切相关的多种生物学功能,TG小鼠疾病进展期脊髓和脑中105种重叠的差异表达蛋白质与122条通路密切相关。参与一组分子功能的差异表达蛋白质在维持神经细胞存活中起重要作用。

结论

本研究提供了TG小鼠额外的蛋白质组学概况,包括脊髓和脑中可能参与发病机制的重叠蛋白质,以及对ALS发病机制中蛋白质上调和下调的新见解。

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本文引用的文献

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Microglial ferroptotic stress causes non-cell autonomous neuronal death.小胶质细胞铁死亡应激导致非细胞自主性神经元死亡。
Mol Neurodegener. 2024 Feb 5;19(1):14. doi: 10.1186/s13024-023-00691-8.
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Potential proteomic alteration in the brain of Tg(SOD1*G93A)1Gur mice: A new pathogenesis insight of amyotrophic lateral sclerosis.Tg(SOD1*G93A)1Gur 小鼠大脑中的潜在蛋白质组学改变:肌萎缩侧索硬化症的新发病机制见解。
Cell Biol Int. 2022 Sep;46(9):1378-1398. doi: 10.1002/cbin.11842. Epub 2022 Jul 8.
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Considerations on the concept, definition, and diagnosis of amyotrophic lateral sclerosis.
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Preliminary Observation about Alteration of Proteins and Their Potential Functions in Spinal Cord of SOD1 G93A Transgenic Mice.SOD1 G93A 转基因小鼠脊髓蛋白改变及其潜在功能的初步观察
Int J Biol Sci. 2018 Jul 27;14(10):1306-1320. doi: 10.7150/ijbs.26829. eCollection 2018.
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Edaravone (Radicava): A Novel Neuroprotective Agent for the Treatment of Amyotrophic Lateral Sclerosis.依达拉奉(Radicava):一种用于治疗肌萎缩侧索硬化症的新型神经保护剂。
P T. 2018 Jan;43(1):25-28.
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Aldehyde Dehydrogenases 1A2 Expression and Distribution are Potentially Associated with Neuron Death in Spinal Cord of Tg(SOD1*G93A)1Gur Mice.醛脱氢酶1A2的表达与分布可能与转基因(Tg(SOD1*G93A)1Gur)小鼠脊髓中的神经元死亡有关。
Int J Biol Sci. 2017 Apr 10;13(5):574-587. doi: 10.7150/ijbs.19150. eCollection 2017.
8
Expression and Distribution of Arylsulfatase B are Closely Associated with Neuron Death in SOD1 G93A Transgenic Mice.芳香基硫酸酯酶 B 的表达和分布与 SOD1 G93A 转基因小鼠神经元死亡密切相关。
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Changes in the Expression of FUS/TLS in Spinal Cords of SOD1 G93A Transgenic Mice and Correlation with Motor-Neuron Degeneration.SOD1 G93A转基因小鼠脊髓中FUS/TLS表达的变化及其与运动神经元变性的相关性
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The Overexpression of TDP-43 Protein in the Neuron and Oligodendrocyte Cells Causes the Progressive Motor Neuron Degeneration in the SOD1 G93A Transgenic Mouse Model of Amyotrophic Lateral Sclerosis.在超氧化物歧化酶1(SOD1)G93A转基因肌萎缩侧索硬化小鼠模型中,神经元和少突胶质细胞中TDP - 43蛋白的过表达导致进行性运动神经元变性。
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