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• W2053443135 endingPage "e108662" @default.
• W2053443135 startingPage "e108662" @default.
• W2053443135 abstract "Bone-marrow-derived mesenchymal stromal cells (MSCs) have the potential to significantly contribute to skeletal muscle healing through the secretion of paracrine factors that support proliferation and enhance participation of the endogenous muscle stem cells in the process of repair/regeneration. However, MSC-derived trophic molecules have been poorly characterized. The aim of this study was to investigate paracrine signaling effects of MSCs on skeletal myoblasts. It was found, using a biochemical and morphological approach that sphingosine 1-phosphate (S1P), a natural bioactive lipid exerting a broad range of muscle cell responses, is secreted by MSCs and represents an important factor by which these cells exert their stimulatory effects on C2C12 myoblast and satellite cell proliferation. Indeed, exposure to conditioned medium obtained from MSCs cultured in the presence of the selective sphingosine kinase inhibitor (iSK), blocked increased cell proliferation caused by the conditioned medium from untreated MSCs, and the addition of exogenous S1P in the conditioned medium from MSCs pre-treated with iSK further increased myoblast proliferation. Finally, we also demonstrated that the myoblast response to MSC-secreted vascular endothelial growth factor (VEGF) involves the release of S1P from C2C12 cells. Our data may have important implications in the optimization of cell-based strategies to promote skeletal muscle regeneration." @default.
• W2053443135 created "2016-06-24" @default.
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• W2053443135 date "2014-09-29" @default.
• W2053443135 modified "2023-09-25" @default.
• W2053443135 title "Mesenchymal Stromal Cell Secreted Sphingosine 1-Phosphate (S1P) Exerts a Stimulatory Effect on Skeletal Myoblast Proliferation" @default.
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• W2053443135 doi "https://doi.org/10.1371/journal.pone.0108662" @default.
• W2053443135 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4181304" @default.
• W2053443135 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/25264785" @default.
• W2053443135 hasPublicationYear "2014" @default.
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