sphingosine-phosphorylcholine and Arteriosclerosis
sphingosine-phosphorylcholine has been researched along with Arteriosclerosis* in 3 studies
Other Studies
3 other study(ies) available for sphingosine-phosphorylcholine and Arteriosclerosis
Article | Year |
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Suppression of endothelial cell apoptosis by high density lipoproteins (HDL) and HDL-associated lysosphingolipids.
Apoptotic cell death following injury of vascular endothelium is assumed to play an important role in the pathogenesis of atherosclerosis. In this report, we demonstrate that high density lipoproteins (HDL), a major anti-atherogenic lipoprotein fraction, protect endothelial cells against growth factor deprivation-induced apoptosis. HDL blocked the mitochondrial pathway of apoptosis by inhibiting dissipation of mitochondrial potential (Deltapsi(m)), generation of reactive oxygen species, and release of cytochrome c into the cytoplasm. As a consequence, HDL prevented activation of caspases 9 and 3 and apoptotic alterations of the plasma membrane such as increase of permeability and translocation of phosphatidylserine. Treatment of endothelial cells with HDL induced activation of the protein kinase Akt, an ubiquitous transducer of anti-apoptotic signals, and led to phosphorylation of BAD, a major Akt substrate. Suppression of Akt activity both by wortmannin and LY-294002 or by a dominant negative Akt mutant abolished the anti-apoptotic effect of HDL. Two bioactive lysosphingolipids present in HDL particles, sphingosylphosphorylcholine and lysosulfatide, fully mimicked the survival effect of HDL by blocking the mitochondrial pathway of apoptosis and potently activating Akt. In conclusion, the present study identifies HDL as a carrier of endogenous endothelial survival factors and suggests that inhibition of endothelial apoptosis by HDL-associated lysosphingolipids may represent an important and novel aspect of the anti-atherogenic activity of HDL. Topics: Apoptosis; Arteriosclerosis; Cell Survival; Cells, Cultured; Endothelium, Vascular; Humans; Lipoproteins, HDL; Mitochondria; Phosphatidylinositol 3-Kinases; Phosphorylcholine; Protein Serine-Threonine Kinases; Proto-Oncogene Proteins; Proto-Oncogene Proteins c-akt; Psychosine; Sphingosine | 2001 |
Immunology. The push-me pull-you of T cell activation.
Topics: Animals; Antigen Presentation; Antigens; Arteriosclerosis; B-Lymphocytes; Cell Cycle Proteins; Humans; Ligands; Lipoproteins, LDL; Lupus Erythematosus, Systemic; Lymphocyte Activation; Lysophosphatidylcholines; Mice; Phosphorylcholine; Receptors, Cell Surface; Receptors, G-Protein-Coupled; Sphingosine; T-Lymphocytes | 2001 |
Lysophosphatidylcholine as a ligand for the immunoregulatory receptor G2A.
Although the biological actions of the cell membrane and serum lipid lysophosphatidylcholine (LPC) in atherosclerosis and systemic autoimmune disease are well recognized, LPC has not been linked to a specific cell-surface receptor. We show that LPC is a high-affinity ligand for G2A, a lymphocyte-expressed G protein-coupled receptor whose genetic ablation results in the development of autoimmunity. Activation of G2A by LPC increased intracellular calcium concentration, induced receptor internalization, activated ERK mitogen-activated protein kinase, and modified migratory responses of Jurkat T lymphocytes. This finding implicates a role for LPC-G2A interaction in the etiology of inflammatory autoimmune disease and atherosclerosis. Topics: Animals; Arteriosclerosis; Calcium; Cell Cycle Proteins; Cell Line; Chemotaxis, Leukocyte; Humans; Jurkat Cells; Ligands; Lupus Erythematosus, Systemic; Lymphocyte Activation; Lysophosphatidylcholines; Mitogen-Activated Protein Kinases; Phosphorylcholine; Radioligand Assay; Receptors, Cell Surface; Receptors, G-Protein-Coupled; Recombinant Fusion Proteins; Signal Transduction; Sphingosine; T-Lymphocytes; Tetradecanoylphorbol Acetate; Transfection; Virulence Factors, Bordetella | 2001 |