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KLF5 通过经典的 Wnt/β-catenin 信号通路调节鸡骨骼肌萎缩。

KLF5 regulates chicken skeletal muscle atrophy via the canonical Wnt/β-catenin signaling pathway.

机构信息

Farm Animal Genetic Resources Exploration and Innovation Key Laboratory of Sichuan Province, Sichuan Agricultural University, 211 Huiming Road, Wenjiang, Sichuan province, Chengdu 611130, China.

Animal Breeding and Genetics Key Laboratory of Sichuan Province, 7 Niusha Road, Jinjiang, Sichuan province, Chengdu 610066, China.

出版信息

Exp Anim. 2020 Nov 12;69(4):430-440. doi: 10.1538/expanim.20-0046. Epub 2020 Jul 7.

DOI:10.1538/expanim.20-0046
PMID:32641593
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7677084/
Abstract

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.

摘要

最近在小鼠中的研究表明,KLF5(Kruppel 样因子 5),一种锌指转录因子,在骨骼肌发育和再生中发挥重要作用。作为肌肉发育过程中的一个重要因素,KLF5 参与调节细胞周期、细胞存活和不同环境条件下的细胞干性,但尚不清楚 KLF5 是否参与肌肉萎缩。因此,我们研究了 KLF5 是否可以调节体外鸡卫星细胞的萎缩,并研究了其作用机制。qPCR 显示,KLF5 基因敲低促进了肌肉萎缩关键基因的表达。随后,我们对 KLF5 沉默和对照细胞的转录组进行了测序和分析,结果表明差异表达基因主要富集在 10 个信号通路中(P<0.05),差异基因和富集分析表明 Wnt 信号通路非常重要。总之,我们的结果表明,KLF5 可能通过 Wnt/β-catenin 信号通路调节鸡骨骼肌的萎缩。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f5e8/7677084/eb99e540534c/expanim-69-430-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f5e8/7677084/07d2a90448a7/expanim-69-430-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f5e8/7677084/efa99390abeb/expanim-69-430-g002.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f5e8/7677084/1d52bfa15f5e/expanim-69-430-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f5e8/7677084/a3c356daf8fe/expanim-69-430-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f5e8/7677084/925d64e1c94c/expanim-69-430-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f5e8/7677084/d988b481c056/expanim-69-430-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f5e8/7677084/e58d11be3bae/expanim-69-430-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f5e8/7677084/eb99e540534c/expanim-69-430-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f5e8/7677084/07d2a90448a7/expanim-69-430-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f5e8/7677084/efa99390abeb/expanim-69-430-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f5e8/7677084/5defd3310630/expanim-69-430-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f5e8/7677084/9deffb54644d/expanim-69-430-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f5e8/7677084/1d52bfa15f5e/expanim-69-430-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f5e8/7677084/a3c356daf8fe/expanim-69-430-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f5e8/7677084/925d64e1c94c/expanim-69-430-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f5e8/7677084/d988b481c056/expanim-69-430-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f5e8/7677084/e58d11be3bae/expanim-69-430-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f5e8/7677084/eb99e540534c/expanim-69-430-g010.jpg

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