The role of FPR2/ALX in the vascular wall

摘要: Cardiovascular diseases caused by atherosclerosis are a leading cause of mortality worldwide. Inflammation has been described as key component in the development atherosclerosis. Lipoxin A4 (LXA4) is lipid mediator derived from arachidonic acid, which anti-inflammatory and proresolution properties mediated through FPR2/ALX receptor. This receptor however, not specific to LXA4 can transduce pro-inflammation or pro-resolution effects depending on different ligands present atherosclerotic milieu. The aim thesis was unravel role signaling vascular wall. In addition, were examined with 2 goals: assess use possible therapeutic option mouse models atherosclerosis, elucidate if signaling. To this end, vivo, vitro ex vivo experiments used evaluate human samples mice either expressing lacking murine homologue (Fpr2). It discovered that macrophages, smooth muscle cells endothelial lesions expressed it up-regulated pro-inflammatory stimuli monocytes vitro. three models, Fpr2 deletion resulted decreased Macrophages knock-out exhibited reduced inflammation dysfunction. Finally, treatment aspirin-triggered (ATL, analogue) significantly cell migration intimal hyperplasia after carotid ligation vivo. Since effect absent mice, supports transduces response mediator. summary, results suggest dual for property disease develops; whereas induced LXA4. differential types within lesion. conclusion, major wall crucial development. well restenosis. ISBN 978-91-7676-092-5 From DEPARTMENT OF MEDICINE, TRANSLATIONAL CARDIOLOGY Karolinska Institutet, Stockholm, Sweden THE ROLE IN VASCULAR WALL