The role of sphingosine-1-phosphate in endothelial barrier function |
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Authors: | Brent A. Wilkerson Kelley M. Argraves |
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Affiliation: | Department of Regenerative Medicine and Cell Biology, Medical University of South Carolina, 173 Ashley Ave., BSB650, Charleston, SC 29425, USA |
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Abstract: | Loss of endothelial barrier function is implicated in the etiology of metastasis, atherosclerosis, sepsis and many other diseases. Studies suggest that sphingosine-1-phosphate (S1P), particularly HDL-bound S1P (HDL–S1P) is essential for endothelial barrier homeostasis and that HDL–S1P may be protective against the loss of endothelial barrier function in disease. This review summarizes evidence providing mechanistic insights into how S1P maintains endothelial barrier function, highlighting the recent findings that implicate the major S1P carrier, HDL, in the maintenance of the persistent S1P-signaling needed to maintain endothelial barrier function. We review the mechanisms proposed for HDL maintenance of persistent S1P-signaling, the evidence supporting these mechanisms and the remaining fundamental questions. |
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Keywords: | S1P, sphingosine-1-phosphate HDL&ndash S1P, HDL-bound S1P albumin&ndash S1P, albumin-bound S1P AKT, protein kinase B SPHK, sphingosine kinase PI3K, phosphatidylinositol 3-kinase S1PR1-3, S1P receptor 1&ndash 3 RAC-1, ras-related C3 botulinum toxin substrate 1 SGC, soluble guanylate cyclase TIAM1, T-cell lymphoma invasion and metastasis 1 APOM, apolipoprotein M TRIP6, TRIP6 thyroid hormone receptor interactor 6 NHERF-2, Na+/H+ exchanger regulatory factor-2 ARP, actin-related protein GPCR, G protein-coupled receptor RHOA, ras homologue family member A VE-cadherin, vascular endothelial cadherin/cadherin 5 |
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