Paraoxonase-2 Modulates Stress Response of Endothelial Cells to Oxidized Phospholipids and a Bacterial Quorum–Sensing Molecule

• DOI: 10.1161/atvbaha.111.232827
• Publication Date: 2011-08-12T01:02:26Z
• Authors: Juyong Brian Kim; Yu-Rong Xia; Casey E. Romanoski; Sangderk Lee; YongHong Meng; Yi-Shou Shi; Noam Bourquard; Ke Wei Gong; Zachary Port; Victor Grijalva; Srinivasa T. Reddy; Judith A. Berliner; Aldons J. Lusis; Diana M. Shih
• Keywords: Homoserine; Cell Signaling; Proinflammatory cytokine; GAS6

Chronic infection has long been postulated as a stimulus for atherogenesis. Pseudomonas aeruginosa associated with increased atherosclerosis in rats, and these bacteria produce quorum-sensing molecule 3-oxo-dodecynoyl-homoserine lactone (3OC12-HSL) that is critical colonization virulence. Paraoxonase 2 (PON2) hydrolyzes 3OC12-HSL also protects against the effects of oxidized phospholipids thought to contribute atherosclerosis. We now report response human aortic endothelial cells (HAECs) 1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphocholine (Ox-PAPC) relation PON2 expression.Using expression profiling network modeling, we identified unfolded protein (UPR), cell cycle genes, mitogen-activated kinase signaling pathway be heavily involved HAEC 3OC12-HSL. The showed striking similarities created based on Ox-PAPC, major component minimally modified low-density lipoprotein. HAECs which was silenced by small interfering RNA proinflammatory UPR when treated or Ox-PAPC.3OC12-HSL Ox-PAPC influence similar inflammatory pathways. Quorum sensing molecules, such 3OC12-HSL, proatherogenic chronic infection. antiatherogenic include destruction quorum molecules.