GSK3 regulation Wnt/β-catenin signaling affects adipogenesis in bovine skeletal muscle fibro/adipogenic progenitors

文献类型： 外文期刊

第一作者： Zhang, Junfang

作者： Zhang, Junfang;Peng, Yinghua;Zhang, Junfang;Wang, Enze;Li, Qiang;Jin, Huaina;Naseem, Sajida;Sun, Bin;Li, Xiangzi;Choi, Seongho;Park, Sungkwon

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关键词： Single -nucleus RNA-sequencing; Wnt/ beta-catenin signaling; Glycogen synthase kinase 3; Fibro/adipogenic progenitor; Intramuscular fat

期刊名称：INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES （ 影响因子：7.7； 五年影响因子：7.7 ）

ISSN： 0141-8130

年卷期： 2024 年 275 卷

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收录情况： SCI

摘要： Clarifying the cellular origin and regulatory mechanisms of intramuscular fat (IMF) deposition is crucial for improving beef quality. Here, we used single-nucleus RNA sequencing to analyze the structure and heterogeneity of skeletal muscle cell populations in different developmental stages of Yanbian cattle and identified eight cell types in two developmental stages of calves and adults. Among them, fibro/adipogenic progenitors (FAPs) expressing CD29 (ITGA7)pos and CD56 (NCAM1)neg surface markers were committed to IMF deposition in beef cattle and expressed major Wnt ligands and receptors. LY2090314/XAV-939 was used to activate/inhibit Wnt/ beta-catenin signal. The results showed that the blockade of Glycogen Synthase Kinase 3 (GSK3) by LY2090314 promoted the stabilization of beta-catenin and reduced the expression of genes related adipogenic differentiation (e. g., PPAR gamma and C/EBP alpha) in bovine FAPs, confirming the anti-adipogenic effect of GSK3. XAV-939 inhibition of the Wnt/beta-catenin pathway promoted the lipid accumulation capacity of FAPs. Furthermore, we found that blocking GSK3 enhanced the paracrine effects of FAPs-MuSCs and increased myotube formation in muscle satellite cells (MuSCs). Overall, our results outline a single-cell atlas of skeletal muscle development in Yanbian cattle, revealed the role of Wnt/GSK3/beta-catenin signaling in FAPs adipogenesis, and provide a theoretical basis for further regulation of bovine IMF deposition.

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