Delta样非典型notch配体2通过Wnt/β-catenin信号通路调节绵羊肌母细胞的增殖和分化。

IF 4.5 2区 生物学 Q2 CELL BIOLOGY
Lixia Sun, Chao Yuan, Xuejiao An, Lingying Kong, Dan Zhang, Bowen Chen, Zengkui Lu, Jianbin Liu
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引用次数: 0

摘要

这项研究深入探讨了δ样非典型notch配体2(DLK2)在肌母细胞的细胞周期、增殖、凋亡和分化中的作用,以及它与经典Wnt/β-catenin信号通路在调控肌母细胞功能中的相互作用。研究发现,在增殖期上调肌母细胞中的DLK2可增强肌母细胞增殖,促进细胞周期进展,减少细胞凋亡。相反,在分化期使用 siRNA 下调 DLK2 的表达则能促进肌母细胞肥大和融合,抑制肌纤维降解因子的表达,加快分化过程。DLK2通过影响与Wnt/β-catenin信号通路相关的各种因素(包括CTNNB1、FZD1、FZD6、RSPO1、RSPO4、WNT4、WNT5A和腺瘤性息肉病大肠杆菌)的表达来调节成肌细胞的功能。从本质上讲,DLK2 在 Wnt/β-catenin 信号通路的参与下,在成肌细胞的细胞周期、增殖、凋亡和分化过程中发挥着重要的调控作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Delta-like noncanonical notch ligand 2 regulates the proliferation and differentiation of sheep myoblasts through the Wnt/β-catenin signaling pathway.

This study delved into the role of delta-like noncanonical notch ligand 2 (DLK2) in the cell cycle, proliferation, apoptosis, and differentiation of myoblasts, as well as its interaction with the classical Wnt/β-catenin signaling pathway in regulating myoblast function. The research revealed that upregulation of DLK2 in myoblasts during the proliferation phase enhanced myoblast proliferation, facilitated cell cycle progression, and reduced apoptosis. Conversely, downregulation of DLK2 expression using siRNA during the differentiation phase promoted myoblast hypertrophy and fusion, suppressed the expression of muscle fiber degradation factors, and expedited the differentiation process. DLK2 regulates myoblasts function by influencing the expression of various factors associated with the Wnt/β-catenin signaling pathway, including CTNNB1, FZD1, FZD6, RSPO1, RSPO4, WNT4, WNT5A, and adenomatous polyposis coli. In essence, DLK2, with the involvement of the Wnt/β-catenin signaling pathway, plays a crucial regulatory role in the cell cycle, proliferation, apoptosis, and differentiation of myoblasts.

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来源期刊
CiteScore
14.70
自引率
0.00%
发文量
256
审稿时长
1 months
期刊介绍: The Journal of Cellular Physiology publishes reports of high biological significance in areas of eukaryotic cell biology and physiology, focusing on those articles that adopt a molecular mechanistic approach to investigate cell structure and function. There is appreciation for the application of cellular, biochemical, molecular and in vivo genetic approaches, as well as the power of genomics, proteomics, bioinformatics and systems biology. In particular, the Journal encourages submission of high-interest papers investigating the genetic and epigenetic regulation of proliferation and phenotype as well as cell fate and lineage commitment by growth factors, cytokines and their cognate receptors and signal transduction pathways that influence the expression, integration and activities of these physiological mediators. Similarly, the Journal encourages submission of manuscripts exploring the regulation of growth and differentiation by cell adhesion molecules in addition to the interplay between these processes and those induced by growth factors and cytokines. Studies on the genes and processes that regulate cell cycle progression and phase transition in eukaryotic cells, and the mechanisms that determine whether cells enter quiescence, proliferate or undergo apoptosis are also welcomed. Submission of papers that address contributions of the extracellular matrix to cellular phenotypes and physiological control as well as regulatory mechanisms governing fertilization, embryogenesis, gametogenesis, cell fate, lineage commitment, differentiation, development and dynamic parameters of cell motility are encouraged. Finally, the investigation of stem cells and changes that differentiate cancer cells from normal cells including studies on the properties and functions of oncogenes and tumor suppressor genes will remain as one of the major interests of the Journal.
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