| http://purl.uniprot.org/citations/17885219 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/17885219 | http://www.w3.org/2000/01/rdf-schema#comment | "Atherosclerosis is a chronic inflammatory disease and represents the major cause of cardiovascular morbidity and mortality. A critical regulator of inflammatory processes represents the mitogen-activated protein kinase-activated protein kinase-2 (MK2). Therefore, we investigated the functional role of MK2 in atherogenesis in hypercholesterolemic mice as well as potentially underlying mechanisms in vivo and in vitro. Activation of MK2 (phospho-MK2) was predominantly detected in the endothelium and macrophage-rich plaque areas within aortas of hypercholesterolemic LDL receptor-deficient mice (ldlr(-/-)). Systemic MK2 deficiency of hypercholesterolemic ldlr(-/-) mice (ldlr(-/-)/mk2(-/-)) significantly decreased the accumulation of lipids and macrophages in the aorta after feeding an atherogenic diet for 8 and 16 weeks despite a significant increase in proatherogenic plasma lipoproteins compared with ldlr(-/-) mice. Deficiency of MK2 significantly decreased oxLDL-induced foam cell formation in vitro, diet-induced foam cell formation in vivo, and expression of scavenger receptor A in primary macrophages. In addition, systemic MK2 deficiency of hypercholesterolemic ldlr(-/-) mice significantly decreased the aortic expression of the adhesion molecule VCAM-1 and the chemokine MCP-1, key mediators of macrophage recruitment into the vessel wall. Furthermore, silencing of MK2 in endothelial cells by siRNA reduced the IL-1beta-induced expression of VCAM-1 and MCP-1. MK2 critically promotes atherogenesis by fostering foam cell formation and recruitment of monocytes/macrophages into the vessel wall. Therefore, MK2 might represent an attractive novel target for the treatment of atherosclerotic cardiovascular disease."xsd:string |
| http://purl.uniprot.org/citations/17885219 | http://purl.org/dc/terms/identifier | "doi:10.1161/circresaha.107.156075"xsd:string |
| http://purl.uniprot.org/citations/17885219 | http://purl.uniprot.org/core/author | "Gaestel M."xsd:string |
| http://purl.uniprot.org/citations/17885219 | http://purl.uniprot.org/core/author | "Drexler H."xsd:string |
| http://purl.uniprot.org/citations/17885219 | http://purl.uniprot.org/core/author | "Schieffer B."xsd:string |
| http://purl.uniprot.org/citations/17885219 | http://purl.uniprot.org/core/author | "Tietge U.J."xsd:string |
| http://purl.uniprot.org/citations/17885219 | http://purl.uniprot.org/core/author | "Bavendiek U."xsd:string |
| http://purl.uniprot.org/citations/17885219 | http://purl.uniprot.org/core/author | "Jagavelu K."xsd:string |
| http://purl.uniprot.org/citations/17885219 | http://purl.uniprot.org/core/date | "2007"xsd:gYear |
| http://purl.uniprot.org/citations/17885219 | http://purl.uniprot.org/core/name | "Circ Res"xsd:string |
| http://purl.uniprot.org/citations/17885219 | http://purl.uniprot.org/core/pages | "1104-1112"xsd:string |
| http://purl.uniprot.org/citations/17885219 | http://purl.uniprot.org/core/title | "Systemic deficiency of the MAP kinase-activated protein kinase 2 reduces atherosclerosis in hypercholesterolemic mice."xsd:string |
| http://purl.uniprot.org/citations/17885219 | http://purl.uniprot.org/core/volume | "101"xsd:string |
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