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10.1096/fj.06-7439com http://scihub22266oqcxt.onion/10.1096/fj.06-7439com C4864469!4864469 !17218539     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=17218539 &cmd=llinks): Failed to open stream: HTTP request failed! 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Hypochlorite-modified albumin colocalizes with RAGE in the artery wall and promotes MCP-1 expression via the RAGE-Erk1/2 MAP-kinase pathway |pdf=|usr=}}{{17218539 }} gab.com Text Hypochlorite-modified albumin colocalizes with RAGE in the artery wall and promotes MCP-1 expression via the RAGE-Erk1/2 MAP-kinase pathway JO: FASEB J http://www.kidney.de/pget.php?&tw=1&pmid=17218539 #FOAvip Signal transduction via the endothelial receptor for advanced glycation end products (RAGE) plays a key role in vascular inflammation. Recent observations have shown that the myeloperoxidase-H2O2-chloride system of activated phagocytes is highly up-regulated under inflammatory conditions where hypochlorous acid (HOCl) is formed as the major oxidant. Albumin, an in vivo carrier for myeloperoxidase is highly vulnerable to oxidation and a major representative of circulating advanced oxidized proteins during inflammatory diseases. Immunohistochemical studies performed in the present study revealed marked colocalization of HOCl-modified epitopes with RAGE and albumin in sections of human atheroma, mainly at the endothelial lining. We show that albumin modified with physiologically relevant concentrations of HOCl, added as reagent or generated by the myeloperoxidase-H2O2-chloride system, is a high affinity ligand for RAGE. Albumin, modified by HOCl in the absence of free amino acids/carbohydrates/lipids to exclude formation of AGE-like structures, induced a rapid, RAGE-dependent activation of extracellular signal-regulated kinase 1/2 and up-regulation of the proinflammatory mediator monocyte chemoattractant protein-1. Cellular activation could be blocked either by a specific polyclonal anti-RAGE IgG and/or a specific mitogen-activated protein-kinase kinase inhibitor. The present study demonstrates that HOCl-modified albumin acts as a ligand for RAGE and promotes RAGE-mediated inflammatory complications. Twit Text FOAVip Hypochlorite-modified albumin colocalizes with RAGE in the artery wall and promotes MCP-1 expression via the RAGE-Erk1/2 MAP-kinase pathway ????FASEB J http://www.kidney.de/pget.php?&tw=1&pmid=17218539 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=17218539 #FOAvip English Wikipedia <ref>{{Cite pmid|17218539 }}</ref> Hypochlorite-modified albumin colocalizes with RAGE in the artery wall and promotes MCP-1 expression via the RAGE-Erk1/2 MAP-kinase pathway #MMPMID17218539 Marsche G ; Semlitsch M ; Hammer A ; Frank S ; Weigle B ; Demling N ; Schmidt K ; Windischhofer W ; Waeg G ; Sattler W ; Malle E FASEB J 2007[Apr]; 21 (4 ): 1145-52 PMID17218539 show ga Signal transduction via the endothelial receptor for advanced glycation end products (RAGE) plays a key role in vascular inflammation. Recent observations have shown that the myeloperoxidase-H2O2-chloride system of activated phagocytes is highly up-regulated under inflammatory conditions where hypochlorous acid (HOCl) is formed as the major oxidant. Albumin, an in vivo carrier for myeloperoxidase is highly vulnerable to oxidation and a major representative of circulating advanced oxidized proteins during inflammatory diseases. Immunohistochemical studies performed in the present study revealed marked colocalization of HOCl-modified epitopes with RAGE and albumin in sections of human atheroma, mainly at the endothelial lining. We show that albumin modified with physiologically relevant concentrations of HOCl, added as reagent or generated by the myeloperoxidase-H2O2-chloride system, is a high affinity ligand for RAGE. Albumin, modified by HOCl in the absence of free amino acids/carbohydrates/lipids to exclude formation of AGE-like structures, induced a rapid, RAGE-dependent activation of extracellular signal-regulated kinase 1/2 and up-regulation of the proinflammatory mediator monocyte chemoattractant protein-1. Cellular activation could be blocked either by a specific polyclonal anti-RAGE IgG and/or a specific mitogen-activated protein-kinase kinase inhibitor. The present study demonstrates that HOCl-modified albumin acts as a ligand for RAGE and promotes RAGE-mediated inflammatory complications. |*Gene Expression Regulation [MESH] |*Inflammation [MESH] |Albumins/*chemistry [MESH] |Arteries/*metabolism [MESH] |Cell Line [MESH] |Chemokine CCL2/*biosynthesis [MESH] |Humans [MESH] |Hypochlorous Acid/*pharmacology [MESH] |MAP Kinase Signaling System [MESH] |Mitogen-Activated Protein Kinase 1/metabolism [MESH] |Mitogen-Activated Protein Kinase 3/metabolism [MESH] |Peroxidase/*metabolism [MESH] |Receptor for Advanced Glycation End Products [MESH] |Receptors, Immunologic/*metabolism [MESH]Hypochlorite-modified albumin colocalizes with RAGE in the artery wall(epmc).pdf DeepDyve Pubget Overpricing