Bioinformatics analysis of paravertebral muscles atrophy in adult degenerative scoliosis.

IF 1.8 3区生物学 Q4 CELL BIOLOGY

Journal of Muscle Research and Cell Motility Pub Date : 2023-12-01 Epub Date: 2023-05-20 DOI:10.1007/s10974-023-09650-8

Zhigang Rong, Zhong Yang, Chengmin Zhang, Rongxi Pu, Can Chen, Jianzhong Xu, Fei Luo

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引用次数: 0

Abstract

Paravertebral muscles (PVM) act as one of the major dynamic factors to maintain human upright activities and play a remarkable role in maintaining the balance of the trunk. Adult degenerative scoliosis (ADS) has become one of the important causes of disability in the elderly population owing to the changes in spinal biomechanics, atrophy and degeneration of PVM, and imbalance of the spine. Previously, many studies focused on the physical evaluation of PVM degeneration. However, the molecular biological changes are still not completely known. In this study, we established a rat model of scoliosis and performed the proteomic analysis of the PVM of ADS. The results showed that the degree of atrophy, muscle fat deposition, and fibrosis of the PVM of rats positively correlated with the angle of scoliosis. The proteomic results showed that 177 differentially expressed proteins were present in the ADS group, which included 105 upregulated proteins and 72 downregulated proteins compared with the PVM in individuals without spinal deformities. Through the construction of a protein-protein interaction network, 18 core differentially expressed proteins were obtained, which included fibrinogen beta chain, apolipoprotein E, fibrinogen gamma chain, thrombospondin-1, integrin alpha-6, fibronectin-1, platelet factor 4, coagulation factor XIII A chain, ras-related protein Rap-1b, platelet endothelial cell adhesion molecule 1, complement C1q subcomponent subunit A, cathepsin G, myeloperoxidase, von Willebrand factor, integrin beta-1, integrin alpha-1, leukocyte surface antigen CD47, and complement C1q subcomponent subunit B. Further analysis of the Kyoto Encyclopedia of Genes and Genomes pathway (KEGG) and immunofluorescence showed that the neutrophil extracellular traps (NETs) formation signaling pathway plays a major role in the pathogenesis of PVM degeneration in ADS. The results of the present study preliminarily laid the molecular biological foundation of PVM atrophy in ADS, which will provide a new therapeutic target for alleviating PVM atrophy and decreasing the occurrence of scoliosis.

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查看原文本刊更多论文

成人退行性脊柱侧凸椎旁肌萎缩的生物信息学分析。

椎旁肌肉(PVM)是维持人体直立活动的主要动力因素之一，在维持躯干平衡方面发挥着显著的作用。成人退行性脊柱侧凸(Adult degenerative scoliosis, ADS)由于脊柱生物力学改变、PVM萎缩退变、脊柱不平衡等原因，已成为老年人致残的重要原因之一。以前，许多研究集中在PVM退变的物理评价上。然而，分子生物学上的变化仍不完全清楚。本研究建立大鼠脊柱侧凸模型，对ADS的PVM进行蛋白质组学分析，结果显示大鼠PVM的萎缩程度、肌肉脂肪沉积、纤维化程度与脊柱侧凸角度呈正相关。蛋白质组学结果显示，与无脊柱畸形的PVM个体相比，ADS组存在177种差异表达蛋白，其中105种蛋白上调，72种蛋白下调。通过构建蛋白-蛋白相互作用网络，获得18个核心差异表达蛋白，包括纤维蛋白原β链、载脂蛋白E、纤维蛋白原γ链、血小板反应蛋白1、整合素α -6、纤维连接素1、血小板因子4、凝血因子XIII a链、ras相关蛋白Rap-1b、血小板内皮细胞粘附分子1、补体C1q亚组分亚基a、组织蛋白酶G、髓过氧化物酶、血管性血友病因子、整合素β -1、整合素α -1、白细胞表面抗原CD47、补体C1q亚组分亚基b进一步分析京都基因基因组百科(KEGG)和免疫荧光分析表明，中性粒细胞胞外陷阱(NETs)形成信号通路在ADS PVM变性的发病机制中起主要作用，本研究结果初步奠定了ADS PVM萎缩的分子生物学基础。为减轻PVM萎缩，减少脊柱侧凸的发生提供了新的治疗靶点。

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来源期刊

Journal of Muscle Research and Cell Motility 生物-细胞生物学

CiteScore

6.20

自引率

0.00%

发文量

审稿时长

>12 weeks

期刊介绍： The Journal of Muscle Research and Cell Motility has as its main aim the publication of original research which bears on either the excitation and contraction of muscle, the analysis of any one of the processes involved therein, the processes underlying contractility and motility of animal and plant cells, the toxicology and pharmacology related to contractility, or the formation, dynamics and turnover of contractile structures in muscle and non-muscle cells. Studies describing the impact of pathogenic mutations in genes encoding components of contractile structures in humans or animals are welcome, provided they offer mechanistic insight into the disease process or the underlying gene function. The policy of the Journal is to encourage any form of novel practical study whatever its specialist interest, as long as it falls within this broad field. Theoretical essays are welcome provided that they are concise and suggest practical ways in which they may be tested. Manuscripts reporting new mutations in known disease genes without validation and mechanistic insight will not be considered. It is the policy of the journal that cells lines, hybridomas and DNA clones should be made available by the developers to any qualified investigator. Submission of a manuscript for publication constitutes an agreement of the authors to abide by this principle.