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- W2242809383 abstract "Sphingolipid metabolites, have emerged as a new class of potent bioactive molecules, implicated in a variety of cellular processes. In particular, sphingosine-1-phosphate (S1P) the product of sphingosine phosphorylation, through transactivation of five cognate G protein-coupled receptors namely endothelial cell differentiation gene receptors (EDGs/S1P1-5), promotes proliferation, differentiation, enhances cell survival and inhibits apoptosis in different cellular systems. Modulation of sphingolipids and their receptors has been shown in some stroke models to be neuroprotective and anti-inflammatory. We undertook this study to elucidate the role of S1P receptor subtypes and sphinosine kinase (SPHK) in models of brain derived endothelial cells and microglia. We studied mono and co-cultures where endotoxin (LPS) activated microglia stimulate endothelial cell death. After documenting SPHK1/ 2 expression in microglia by immunofluorescence, we found that an agonist of SPHK ((2-(p-Hydrozyanilino)-4(p-chlorophenyl) tiazole, SKI) preserved microvascular endothelial cells, and markedly prevented microglia-induced endothelial cell injury. Furthermore, SKI inhibited iNOS and NO generation in microglia by both endotoxin as well as a second TLR4 agonist (Kdo2-Lipid (ADi[3-deoxy-D-manno-octulosonyl]-lipid A) (*P" @default.
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- W2242809383 date "2012-02-01" @default.
- W2242809383 modified "2023-09-23" @default.
- W2242809383 title "Abstract 2342: Sphingosine Kinase & Sphingosine 1-phosphate Modulation On Microglia And Brain Derived Endothelial Cells" @default.
- W2242809383 hasPublicationYear "2012" @default.
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