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S1P<jats:sub>1<\/jats:sub>R is critical for vascular maturation, with its loss leading to embryonic death by E14.5; however, its function during early cardiac development is not well known. Our previous studies demonstrated that altered S1P levels adversely affects atrioventricular (AV) canal development <jats:italic>in vitro<\/jats:italic>, with reduced levels leading to cell death and elevated levels inhibiting cell migration and endothelial to mesenchymal cell transformation (EMT).<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Results<\/jats:title>\n            <jats:p>We determined, by real-time PCR analysis, that S1P<jats:sub>1<\/jats:sub>R was expressed at least 10-fold higher than other S1P receptors in the developing heart. Immunohistochemical analysis revealed S1P<jats:sub>1<\/jats:sub>R protein expression in both endothelial and myocardial cells in the developing atrium and ventricle. Using AV canal cultures, we observed that treatment with either FTY720 (an S1P<jats:sub>1,3,4,5<\/jats:sub>R agonist) or KRP203 (an S1P<jats:sub>1<\/jats:sub>R-specific agonist) caused similar effects on AV canal cultures as S1P treatment, including induction of cell rounding, inhibition of cell migration, and inhibition of EMT. <jats:italic>In vivo<\/jats:italic>, morphological analysis of embryonic hearts at E10.5 revealed that S1P<jats:sub>1<\/jats:sub>R-\/- hearts were malformed with reduced myocardial tissue. In addition to reduced myocardial tissue, E12.5 S1P<jats:sub>1<\/jats:sub>R-\/- hearts had disrupted morphology of the heart wall and trabeculae, with thickened and disorganized outer compact layer and reduced fibronectin (FN) deposition compared to S1P<jats:sub>1<\/jats:sub>R+\/+ littermates. The reduced myocardium was accompanied by a decrease in cell proliferation but not an increase in apoptosis.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Conclusions<\/jats:title>\n            <jats:p>These data indicate that S1P<jats:sub>1<\/jats:sub>R is the primary mediator of S1P action in AV canal cultures and that loss of S1P<jats:sub>1<\/jats:sub>R expression <jats:italic>in vivo<\/jats:italic> leads to malformed embryonic hearts, in part due to reduced fibronectin expression and reduced cell proliferation.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1186\/1471-213x-11-37","type":"journal-article","created":{"date-parts":[[2011,6,14]],"date-time":"2011-06-14T06:27:34Z","timestamp":1308032854000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":13,"title":["The Sphingosine-1-phospate receptor 1 mediates S1P action during cardiac development"],"prefix":"10.1186","volume":"11","author":[{"given":"Ryan R","family":"Poulsen","sequence":"first","affiliation":[]},{"given":"Carolyn M","family":"McClaskey","sequence":"additional","affiliation":[]},{"given":"Scott A","family":"Rivkees","sequence":"additional","affiliation":[]},{"given":"Christopher C","family":"Wendler","sequence":"additional","affiliation":[]}],"member":"297","published-online":{"date-parts":[[2011,6,13]]},"reference":[{"key":"638_CR1","doi-asserted-by":"publisher","first-page":"193","DOI":"10.1016\/S1388-1981(02)00341-4","volume":"1585","author":"M Maceyka","year":"2002","unstructured":"Maceyka M, Payne SG, Milstien S, Spiegel S: Sphingosine kinase, sphingosine-1-phosphate, and apoptosis. 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