LncRNA SNHG1 regulates muscle stem cells fate through Wnt/β-catenin pathway.

IF 2 3区生物学 Q2 ANATOMY & MORPHOLOGY

Developmental Dynamics Pub Date : 2025-03-21 DOI:10.1002/dvdy.70017

Changying Wang, Wenwen Wu, Junyi Chen, Heng Wang, Pengxiang Zhao

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引用次数: 0

Abstract

Background: Skeletal muscle stem cells (MuSCs) played an important role in maintaining the proper function of muscle tissues. In adults, they normally remained in a quiescent state and activated upon stimulation to undergo self-renewal or myogenic differentiation. This process was complexly regulated by cytokines, and the molecular mechanisms that promoted MuSCs activation remained largely unknown.

Results: Here, we analyzed transcriptome data from MuSCs activated by different stimuli using weighted gene co-expression network analysis (WGCNA) and identified the key long non-coding RNA SNHG1 (lncSNHG1), which promotes the transition from the quiescent to the activated state of MuSCs. Overexpression of lncSNHG1 was able to promote the proliferation and differentiation of MuSCs, whereas knockdown resulted in the opposite results. Mechanistically, the disruption of the Wnt/β-catenin pathway blocked the quiescence exit induced by lncSNHG1.

Conclusions: We conclude that lncSNHG1 is a key factor that promotes the transition from the quiescent to the activated state of MuSCs and promotes cell proliferation and differentiation through the Wnt/β-catenin pathway.

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LncRNA SNHG1通过Wnt/β-catenin通路调控肌肉干细胞命运。

背景：骨骼肌干细胞（MuSCs）在维持肌肉组织正常功能方面发挥着重要作用。在成人中，它们通常保持静止状态，并在受到刺激时激活以进行自我更新或肌源性分化。这一过程受细胞因子的复杂调控，而促进musc活化的分子机制在很大程度上仍然未知。结果：本研究利用加权基因共表达网络分析（WGCNA）对不同刺激激活的musc转录组数据进行了分析，确定了促进musc从静止状态向激活状态转变的关键长链非编码RNA SNHG1 （lncSNHG1）。lncSNHG1过表达能够促进MuSCs的增殖和分化，而敲低则相反。机制上，Wnt/β-catenin通路的破坏阻断了lncSNHG1诱导的静止退出。结论：我们认为lncSNHG1是通过Wnt/β-catenin通路促进MuSCs从静止状态向激活状态转变，促进细胞增殖分化的关键因子。

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

Developmental Dynamics 生物-发育生物学

CiteScore

5.10

自引率

8.00%

发文量

116

审稿时长

3-8 weeks

期刊介绍： Developmental Dynamics, is an official publication of the American Association for Anatomy. This peer reviewed journal provides an international forum for publishing novel discoveries, using any model system, that advances our understanding of development, morphology, form and function, evolution, disease, stem cells, repair and regeneration.