| http://purl.uniprot.org/citations/16251188 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/16251188 | http://www.w3.org/2000/01/rdf-schema#comment | "We have previously reported (Dobreva, I., Waeber, G., Mooser, V., James, R. W., and Widmann, C. (2003) J. Lipid Res. 44, 2382-2390) that low density lipoproteins (LDLs) induce activation of the p38 MAPK pathway, resulting in fibroblast spreading and lamellipodia formation. Here, we show that LDL-stimulated fibroblast spreading and wound sealing are due to secretion of a soluble factor. Using an antibody-based human protein array, interleukin-8 (IL-8) was identified as the main cytokine whose concentration was increased in supernatants from LDL-stimulated cells. Incubation of supernatants from LDL-treated cells with an anti-IL-8 blocking antibody completely abolished their ability to induce cell spreading and mediate wound closure. In addition, fibroblasts treated with recombinant IL-8 spread to the same extent as cells incubated with LDL or supernatants from LDL-treated cells. The ability of LDL and IL-8 to induce fibroblast spreading was mediated by the IL-8 receptor type II (CXCR-2). Furthermore, LDL-induced IL-8 production and subsequent wound closure required the activation of the p38 MAPK pathway, because both processes were abrogated by a specific p38 inhibitor. Therefore, the capacity of LDLs to induce fibroblast spreading and accelerate wound closure relies on their ability to stimulate IL-8 secretion in a p38 MAPK-dependent manner. Regulation of fibroblast shape and migration by lipoproteins may be relevant to atherosclerosis that is characterized by increased LDL cholesterol levels, IL-8 production, and extensive remodeling of the vessel wall."xsd:string |
| http://purl.uniprot.org/citations/16251188 | http://purl.org/dc/terms/identifier | "doi:10.1074/jbc.m508857200"xsd:string |
| http://purl.uniprot.org/citations/16251188 | http://purl.uniprot.org/core/author | "Waeber G."xsd:string |
| http://purl.uniprot.org/citations/16251188 | http://purl.uniprot.org/core/author | "James R.W."xsd:string |
| http://purl.uniprot.org/citations/16251188 | http://purl.uniprot.org/core/author | "Widmann C."xsd:string |
| http://purl.uniprot.org/citations/16251188 | http://purl.uniprot.org/core/author | "Dobreva I."xsd:string |
| http://purl.uniprot.org/citations/16251188 | http://purl.uniprot.org/core/date | "2006"xsd:gYear |
| http://purl.uniprot.org/citations/16251188 | http://purl.uniprot.org/core/name | "J Biol Chem"xsd:string |
| http://purl.uniprot.org/citations/16251188 | http://purl.uniprot.org/core/pages | "199-205"xsd:string |
| http://purl.uniprot.org/citations/16251188 | http://purl.uniprot.org/core/title | "Interleukin-8 secretion by fibroblasts induced by low density lipoproteins is p38 MAPK-dependent and leads to cell spreading and wound closure."xsd:string |
| http://purl.uniprot.org/citations/16251188 | http://purl.uniprot.org/core/volume | "281"xsd:string |
| http://purl.uniprot.org/citations/16251188 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/16251188 |
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