Recent studies in mice suggested that KLF5 (Kruppel like factor 5), a zinc-finger transcription factor, plays an important role in skeletal muscle development and regeneration. As an important factor in the process of muscle development, KLF5 participates in the regulation of the cell cycle, cell survival, and cell dryness under different environmental conditions, but it is not clear whether KLF5 participates in muscle atrophy. Therefore, we investigated whether KLF5 can regulate the atrophy of chicken satellite cells in vitro and examined its mechanism of action. qPCR showed that KLF5 gene knockdown promoted the expression of key genes in muscle atrophy. Subsequently, we sequenced and analyzed the transcriptomes of KLF5 silenced and control cells, and we showed that the differentially expressed genes were mainly enriched in 10 signaling pathways ( P 0.05), with differential gene and enrichment analyses indicating that the Wnt signaling pathways are extremely important. In conclusion, our results indicate that KLF5 may regulate the atrophy of chicken skeletal muscle through the Wnt/β-catenin signaling pathway.
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机译:近期小鼠的研究表明,KLF5(Kruppel like 5),一种锌 - 手指转录因子,在骨骼肌发育和再生中起重要作用。作为肌肉发育过程中的一个重要因素,KLF5在不同的环境条件下参与细胞周期,细胞存活和细胞干燥的调节,但目前尚不清楚KLF5是否参与肌肉萎缩。因此,我们研究了KLF5是否可以体外调节鸡卫星细胞的萎缩并检查其作用机制。 QPCR显示KLF5基因敲低促进了肌肉萎缩中关键基因的表达。随后,我们测序并分析了KLF5沉默和对照细胞的转录组,并且我们表明差异表达的基因主要富集为10个信号传导途径(P <0.05),具有差异基因和富集分析,表明WNT信号通路非常重要重要的。总之,我们的结果表明,KLF5可以通过Wnt /β-catenin信号通路调节鸡骨骼肌的萎缩。
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