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Fibronectin regulates Wnt7a signaling and satellite cell expansion

ABSTRACT: The influence of the extracellular matrix (ECM) within the stem cell niche remains poorly understood. We found that Syndecan-4 (Sdc4) and Frizzled-7 (Fzd7) form a coreceptor complex in satellite cells and that binding of the ECM glycoprotein Fibronectin (FN) to Sdc4 stimulates the ability of Wnt7a to induce the symmetric expansion of satellite stem cells. Newly activated satellite cells dynamically remodel their niche via transient high-level expression of FN. Knockdown of FN in prospectively isolated satellite cells severely impaired their ability to repopulate the satellite cell niche. Conversely, in vivo overexpression of FN with Wnt7a dramatically stimulated the expansion of satellite stem cells in regenerating muscle. Therefore, activating satellite cells remodel their niche through autologous expression of FN that provides feedback to stimulate Wnt7a signaling through the Fzd7/Sdc4 coreceptor complex. Thus, FN and Wnt7a together regulate the homeostatic levels of satellite stem cells and satellite myogenic cells during regenerative myogenesis.

ORGANISM(S): Mus musculus

PROVIDER: GSE59272 | GEO | 2014/07/11

SECONDARY ACCESSION(S): PRJNA255003

REPOSITORIES: GEO

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Project description:Introduction: Skeletal muscle satellite cells (MuSCs, or stem cells) play a crucial role in muscle development, maintenance, and regeneration, serving both hypertrophic support 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. Methods: This study delves into the emerging challenge of wooden breast (WB) myopathy and its connection to 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 in vitro and in vivo. SDC4 overexpression in MuSCs and blocking peptides corresponding to the SDC4 ectodomain were used for investigation of the role of SDC4 in muscle development and its shedding levels. Results and Discussion: Examination in vivo of affected muscles revealed smaller fibers and changes in metabolic pathways. In vitro studies unveiled disrupted proliferation of MuSCs in WB myopathy, accompanied by downregulation of several muscle markers. Investigation of a potentially 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 decreased proliferation in MuSCs and affected myogenesis. We detected the impairment 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 valuable knowledge on the molecular mechanisms underlying WB myopathy and role of SDC4 in this chicken myopathy.

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Fibronectin regulates Wnt7a signaling and satellite cell expansion

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