ARHGEF9对成肌细胞迁移和分化的影响。

IF 1.8 3区 生物学 Q4 CELL BIOLOGY
Shuang Li, Jin Xu, Wenjia Zhang, Yongze Liu, Huili Tong, Bingchen Liu
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引用次数: 0

摘要

鸟嘌呤核苷酸交换因子9 (Rho guanine nucleotide exchange factor 9, ARHGEF9)作为一种辅助小gtp酶的蛋白,广泛存在于各种组织中。据报道,它主要在神经系统疾病和神经胶质瘤中起重要作用。然而,还没有关于其对损伤后骨骼肌再生影响的报道。本研究首次证实了ARHGEF9蛋白在小鼠损伤后骨骼肌再生过程中的表达显著增加。其次,在小鼠C2C12成肌细胞分化过程中,ARHGEF9显著升高并与肌动蛋白丝共定位。抑制ARHGEF9可显著下调小鼠C2C12成肌细胞的迁移速率和肌动蛋白丝聚合,显著降低细胞迁移相关蛋白的表达。最后,抑制ARHGEF9可显著降低小鼠C2C12成肌细胞的分化能力。综上所述,ARHGEF9对成肌细胞迁移和分化的影响表明,靶向ARHGEF9可能有利于促进骨骼肌的再生和修复。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The influences of ARHGEF9 on myoblasts migration and differentiation.

Rho guanine nucleotide exchange factor 9 (ARHGEF9), as a protein that assists small GTPases, is widely present in various tissues. It has been reported to play an important role mainly in neurological diseases and gliomas. However, there have been no reports on its impact on skeletal muscle regeneration after injury. This study first demonstrated a significant increase in ARHGEF9 protein expression during the regeneration of skeletal muscle post-injury in mice. Secondly, during the differentiation of mouse C2C12 myoblasts, ARHGEF9 significantly increased and co-localized with actin filaments. Inhibition of ARHGEF9 significantly downregulated the migration rate and actin filaments polymerization of mouse C2C12 myoblasts, and significantly reduced the expression of proteins related to cell migration. Finally, inhibition of ARHGEF9 significantly reduced the differentiation ability of mouse C2C12 myoblasts. In summary, ARHGEF9 impacting on myoblasts migration and differentiation suggests that targeting ARHGEF9 could be beneficial for promoting skeletal muscle regeneration and repair.

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来源期刊
CiteScore
6.20
自引率
0.00%
发文量
21
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.
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