ArticleBMC developmental biology2011
The Sphingosine-1-phospate receptor 1 mediates S1P action during cardiac development.
Article in BMC developmental biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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11 citing papers in PubMed, 17 citations in OpenAlex.
- Association of Neurodevelopmental Disorders and Congenital Anomalies With Prenatal Multiple Sclerosis Treatment-Real-World Historical Cohort Study.Clinical pharmacology and therapeutics · 2026Article
- The novel sphingosine-1-phosphate receptor modulator KRP-203 prevents myocardial ischemia-reperfusion injury by preserving mitochondrial function through activation of the RISK and SAFE signaling pathways.Cell biology and toxicology · 2025Article
- The critical role of cardiolipin in metazoan differentiation, development, and maturation.Developmental dynamics : an official publication of the American Association of Anatomists · 2023Review
- S1P receptor modulators and the cardiovascular autonomic nervous system in multiple sclerosis: a narrative review.Therapeutic advances in neurological disorders · 2022Review
- Identification of cardiac hemo-vascular precursors and their requirement of sphingosine-1-phosphate receptor 1 for heart development.Scientific reports · 2017Article
- Sphingosine 1-phosphate receptor-1 in cardiomyocytes is required for normal cardiac development.Developmental biology · 2016Article
- Synergistic effect of bioactive lipid and condition medium on cardiac differentiation of human mesenchymal stem cells from different tissues.Cell biochemistry and function · 2016Article
- The role of sphingosine-1-phosphate in endothelial barrier function.Biochimica et biophysica acta · 2014Review
- Sphingosine kinase and sphingosine 1-phosphate in the heart: a decade of progress.Biochimica et biophysica acta · 2013Review
- Oral available agents in the treatment of relapsing remitting multiple sclerosis: an overview of merits and culprits.Drug, healthcare and patient safety · 2013Article
- Immunohistochemical analysis of sphingosine phosphate lyase expression during murine development.Gene expression patterns : GEPArticle
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
backgroundSphingosine-1-phosophate (S1P) is a biologically active sphingolipid metabolite that influences cellular events including differentiation, proliferation, and migration. S1P acts through five distinct cell surface receptors designated S1P1-5R, with S1P1R having the highest expression level in the developing heart. S1P1R 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 in vitro, with reduced levels leading to cell death and elevated levels inhibiting cell migration and endothelial to mesenchymal cell transformation (EMT).
resultsWe determined, by real-time PCR analysis, that S1P1R was expressed at least 10-fold higher than other S1P receptors in the developing heart. Immunohistochemical analysis revealed S1P1R 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 S1P1,3,4,5R agonist) or KRP203 (an S1P1R-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. In vivo, morphological analysis of embryonic hearts at E10.5 revealed that S1P1R-/- hearts were malformed with reduced myocardial tissue. In addition to reduced myocardial tissue, E12.5 S1P1R-/- hearts had disrupted morphology of the heart wall and trabeculae, with thickened and disorganized outer compact layer and reduced fibronectin (FN) deposition compared to S1P1R+/+ littermates. The reduced myocardium was accompanied by a decrease in cell proliferation but not an increase in apoptosis.
conclusionsThese data indicate that S1P1R is the primary mediator of S1P action in AV canal cultures and that loss of S1P1R expression in vivo leads to malformed embryonic hearts, in part due to reduced fibronectin expression and reduced cell proliferation.
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