Pejšková Lucie, Pisconti Addolorata, Lunde Marianne, Ho Ka Yi, Solberg Nina Therese, Koga Shiori, Tengstrand Erik, Carlson Cathrine Rein, Pedersen Mona Elisabeth, Rønning Sissel Beate
Raw Materials and Optimalization, Nofima AS, Ås, Norway.
Department of Biochemistry and Cell Biology, SUNY Stony Brook, Stony Brook, NY, United States.
Front Physiol. 2024 Dec 23;15:1513311. doi: 10.3389/fphys.2024.1513311. eCollection 2024.
Skeletal muscle satellite cells (MuSCs or stem cells) play a crucial role in muscle development, maintenance, and regeneration, supporting both hypertrophy and regenerative myogenesis. Syndecans (SDCs) act as communication bridges within the muscle microenvironment, regulating interactions with extracellular matrix components and contributing significantly to tissue repair and inflammation. Specifically, syndecan-4 (SDC4) is involved in muscle regeneration at multiple stages.
This study delves into the emerging challenge of wooden breast (WB) myopathy and its connection with SDC4. Our hypothesis proposes that disruptions in MuSC dynamics through SDC4 contribute to the increased incidence of breast myopathies observed in growing broilers. To test our hypothesis, non-affected and affected broilers were systematically selected, and the characteristics of WB myopathy were studied both and . SDC4 overexpression in MuSCs and blocking peptides (BPs) corresponding to the SDC4 ectodomain were used for investigating the role of SDC4 in muscle development and its shedding levels.
examination of affected muscles revealed smaller fibers and changes in metabolic pathways. studies unveiled disrupted proliferation of MuSCs in WB myopathy, accompanied by the downregulation of several muscle markers. Investigation of the potential role of SDC4 in the pathogenesis of WB myopathy revealed a decreased tendency in SDC4 gene expression and increased shedding of its ectodomain. Moreover, we showed that SDC4 overexpression is linked to reduced proliferation in MuSCs and affected myogenesis. We detected an impaired proliferation of WB-affected MuSCs, revealing critical insights into the dysfunctional state of these cells in myopathy. Additionally, by treating MuSCs with blocking peptides derived from the SDC4 ectodomain, we identified altered proliferation. Taken together, this work contributes with valuable knowledge on the molecular mechanisms underlying WB myopathy and the role of SDC4 in this chicken myopathy.
骨骼肌卫星细胞(肌肉卫星细胞或干细胞)在肌肉发育、维持和再生中起关键作用,支持肥大和再生性肌生成。多功能蛋白聚糖(SDCs)在肌肉微环境中充当通讯桥梁,调节与细胞外基质成分的相互作用,并对组织修复和炎症有显著贡献。具体而言,多功能蛋白聚糖-4(SDC4)在多个阶段参与肌肉再生。
本研究深入探讨木胸(WB)肌病这一新兴挑战及其与SDC4的联系。我们的假设提出,通过SDC4对肌肉卫星细胞动态的破坏导致在生长中的肉鸡中观察到的胸肌肌病发病率增加。为了验证我们的假设,系统选择了未受影响和受影响的肉鸡,并对木胸肌病的特征进行了研究。在肌肉卫星细胞中过表达SDC4以及使用与SDC4胞外域对应的阻断肽(BPs)来研究SDC4在肌肉发育中的作用及其脱落水平。
对受影响肌肉的检查发现纤维较小且代谢途径发生变化。研究揭示了木胸肌病中肌肉卫星细胞增殖受到破坏,同时几种肌肉标志物下调。对SDC4在木胸肌病发病机制中的潜在作用的研究表明,SDC4基因表达有下降趋势,其胞外域的脱落增加。此外,我们表明SDC4过表达与肌肉卫星细胞增殖减少和受影响的肌生成有关。我们检测到受木胸影响的肌肉卫星细胞增殖受损,揭示了这些细胞在肌病中功能失调状态的关键见解。此外,通过用源自SDC4胞外域的阻断肽处理肌肉卫星细胞,我们发现增殖发生了改变。综上所述,这项工作为木胸肌病的分子机制以及SDC4在这种鸡肌病中的作用提供了有价值的知识。