The RNA surveillance factor UPF1 regulates the migration and adhesion of porcine skeletal muscle satellite cells.

IF 1.8 3区生物学 Q4 CELL BIOLOGY

Journal of Muscle Research and Cell Motility Pub Date : 2021-06-01 DOI:10.1007/s10974-020-09585-4

Yanjie Tan, Yi Jin, Sheng Wang, Jianhua Cao, Zhuqing Ren

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引用次数: 2

Abstract

Skeletal muscle satellite cells (SCs) play an important role in the repairment and regeneration of damaged muscle. The activation, proliferation, migration, and differentiation of SCs are essential to the response to muscle injury. Up-frameshift 1 (UPF1) is involved in the regulation of many developmental processes. However, the role of UPF1 and its associated regulatory mechanism in SCs are still unclear. Here, we analyzed changes in the transcriptome of porcine SCs with UPF1 knockdown. The results showed that focal adhesion and actin cytoskeleton processes were regulated by UPF1. We also confirmed experimentally that UPF1 promoted SC migration and adhesion by regulating the expression of F-Actin, Vinculin, and several adhesion-related genes. Furthermore, we found that phosphorylated focal adhesion kinase (p-FAK) was down-regulated by UPF1 knockdown. This study identifies the role of UPF1 in regulating SC migration and adhesion and therefore provides new insight into the regulatory mechanism of UPF1 in the process of repairing damaged muscle.

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RNA监视因子UPF1调控猪骨骼肌卫星细胞的迁移和粘附。

骨骼肌卫星细胞在损伤肌肉的修复和再生中起着重要的作用。SCs的激活、增殖、迁移和分化对肌肉损伤的反应至关重要。上移码1 (UPF1)参与了许多发育过程的调控。然而，UPF1在SCs中的作用及其相关调控机制尚不清楚。在这里，我们分析了UPF1敲低的猪SCs转录组的变化。结果表明，UPF1可调控局灶黏附和肌动蛋白细胞骨架过程。我们还通过实验证实，UPF1通过调节F-Actin、Vinculin和几个粘附相关基因的表达来促进SC迁移和粘附。此外，我们发现磷酸化局灶黏附激酶(p-FAK)被UPF1敲除下调。本研究确定了UPF1在调节SC迁移和粘附中的作用，从而为UPF1在损伤肌肉修复过程中的调节机制提供了新的见解。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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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.