Lysophosphatidic acid activates nuclear factor kappa B and induces proinflammatory gene expression in endothelial cells - Palmetshofer, A; Robson, S C; Nehls, V (Thrombosis and haemostasis, 1999)
Keywords: Animals; Cells, Cultured; Chemokine CCL2 - biosynthesis; Chemokine CCL2 - genetics; Drug Synergism; E-Selectin - biosynthesis; E-Selectin - genetics; Endothelium, Vascular - drug effects; Endothelium, Vascular - metabolism; Gene Expression Regulation - drug effects; Inflammation - genetics; Intercellular Adhesion Molecule-1 - biosynthesis; Intercellular Adhesion Molecule-1 - genetics; Interleukin-8 - biosynthesis; Interleukin-8 - genetics; Lysophospholipids - pharmacology; MAP Kinase Signaling System - drug effects; NF-kappa B - metabolism; Quinacrine - pharmacology; Receptors, Cell Surface - antagonists & inhibitors; Receptors, G-Protein-Coupled; Receptors, Lysophosphatidic Acid; Recombinant Proteins - pharmacology; RNA, Messenger - biosynthesis; RNA, Messenger - genetics; Suramin - pharmacology; Swine; Thrombospondins - pharmacology; Transcription, Genetic - drug effects; Tumor Necrosis Factor-alpha - pharmacology