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Publication : Sphingosine 1-phosphate stimulates proliferation and migration of satellite cells: role of S1P receptors.

First Author  Calise S Year  2012
Journal  Biochim Biophys Acta Volume  1823
Issue  2 Pages  439-50
PubMed ID  22178384 Mgi Jnum  J:180663
Mgi Id  MGI:5306823 Doi  10.1016/j.bbamcr.2011.11.016
Citation  Calise S, et al. (2012) Sphingosine 1-phosphate stimulates proliferation and migration of satellite cells Role of S1P receptors. Biochim Biophys Acta 1823(2):439-50
abstractText  Satellite cells are resident stem cells of skeletal muscle; they are normally quiescent but upon post-trauma activation start to proliferate and fuse with damaged fibers contributing to muscle regeneration. In this study the effect of the bioactive sphingolipid sphingosine 1-phosphate (S1P) on the proliferative and migratory response of murine satellite cells has been examined. S1P was found to stimulate labeled thymidine incorporation in a phosphatidylinositol 3-kinase-dependent manner. Moreover, by employing selective S1P receptor agonists and antagonists and silencing individual S1P receptors, the mitogenic action of S1P in satellite cells was shown to depend on S1P(2) and S1P(3). Notably, by using different experimental approaches S1P was found to positively influence satellite cell migration, necessary for their recruitment at the site of muscle damage. Interestingly, the specific silencing of individual S1P receptor subtypes demonstrated the pivotal role of S1P(1) and S1P(4) in mediating the S1P migratory effect. This latter result demonstrates for the first time that S1P(4) receptor has a role in skeletal muscle cells, supporting the notion that this receptor subtype plays a biological action broader than that so far identified in lymphoid tissue. On the contrary, S1P(2) was found to negatively regulate cell migration. Collectively, these results are in favour of an important function of S1P in satellite cell biology that could in principle be exploited as novel pharmacological target for improving skeletal muscle regeneration.
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