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10.1161/ATVBAHA.113.301436 http://scihub22266oqcxt.onion/10.1161/ATVBAHA.113.301436 C3739701!3739701 !23539221     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=23539221 &cmd=llinks): Failed to open stream: HTTP request failed! 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Cocaine and specific cocaine metabolites induce von Willebrand factor release from endothelial cells in a tissue-specific manner |pdf=|usr=}}{{23539221 }} gab.com Text Cocaine and specific cocaine metabolites induce von Willebrand factor release from endothelial cells in a tissue-specific manner JO: Arterioscler Thromb Vasc Biol http://www.kidney.de/pget.php?&tw=1&pmid=23539221 #FOAvip OBJECTIVE: Cocaine use is associated with arterial thrombosis, including myocardial infarction and stroke. Cocaine use results in increased plasma von Willebrand factor (VWF), accelerated atherosclerosis, and platelet-rich arterial thrombi, suggesting that cocaine activates the endothelium, promoting platelet-VWF interactions. APPROACH AND RESULTS: Human umbilical vein endothelial cells, brain microvasculature endothelial cells, or coronary artery endothelial cells were treated with cocaine or metabolites benzoylecgonine, cocaethylene, norcocaine, or ecgonine methylester. Supernatant VWF concentration and multimer structure were measured, and platelet-VWF strings formed on the endothelial surface under flow were quantified. Cocaine, benzoylecgonine, and cocaethylene induced endothelial VWF release, with the 2 metabolites being more potent than the parent molecule. Brain microvasculature endothelial cells were more sensitive to cocaine and metabolites than were human umbilical vein endothelial cells or coronary artery endothelial cells. Coronary artery endothelial cells released VWF into the supernatant but did not form VWF-platelet strings. Intracellular cAMP concentration was not increased after treatment with cocaine or its metabolites. CONCLUSIONS: Both cocaine and metabolites benzoylecgonine and cocaethylene induced endothelial VWF secretion, possibly explaining thrombotic risk after cocaine ingestion. VWF secretion is likely to vary between vascular beds, with brain endothelial cells being particularly sensitive. These results suggest that clinical management of cocaine-induced ischemia may benefit from therapies aimed at disrupting the VWF-platelet interaction. Twit Text FOAVip Cocaine and specific cocaine metabolites induce von Willebrand factor release from endothelial cells in a tissue-specific manner ????Arterioscler Thromb Vasc Biol http://www.kidney.de/pget.php?&tw=1&pmid=23539221 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=23539221 #FOAvip English Wikipedia <ref>{{Cite pmid|23539221 }}</ref> Cocaine and specific cocaine metabolites induce von Willebrand factor release from endothelial cells in a tissue-specific manner #MMPMID23539221 Hobbs WE ; Moore EE ; Penkala RA ; Bolgiano DD ; López JA Arterioscler Thromb Vasc Biol 2013[Jun]; 33 (6 ): 1230-7 PMID23539221 show ga OBJECTIVE: Cocaine use is associated with arterial thrombosis, including myocardial infarction and stroke. Cocaine use results in increased plasma von Willebrand factor (VWF), accelerated atherosclerosis, and platelet-rich arterial thrombi, suggesting that cocaine activates the endothelium, promoting platelet-VWF interactions. APPROACH AND RESULTS: Human umbilical vein endothelial cells, brain microvasculature endothelial cells, or coronary artery endothelial cells were treated with cocaine or metabolites benzoylecgonine, cocaethylene, norcocaine, or ecgonine methylester. Supernatant VWF concentration and multimer structure were measured, and platelet-VWF strings formed on the endothelial surface under flow were quantified. Cocaine, benzoylecgonine, and cocaethylene induced endothelial VWF release, with the 2 metabolites being more potent than the parent molecule. Brain microvasculature endothelial cells were more sensitive to cocaine and metabolites than were human umbilical vein endothelial cells or coronary artery endothelial cells. Coronary artery endothelial cells released VWF into the supernatant but did not form VWF-platelet strings. Intracellular cAMP concentration was not increased after treatment with cocaine or its metabolites. CONCLUSIONS: Both cocaine and metabolites benzoylecgonine and cocaethylene induced endothelial VWF secretion, possibly explaining thrombotic risk after cocaine ingestion. VWF secretion is likely to vary between vascular beds, with brain endothelial cells being particularly sensitive. These results suggest that clinical management of cocaine-induced ischemia may benefit from therapies aimed at disrupting the VWF-platelet interaction. |Brain/cytology [MESH] |Cells, Cultured [MESH] |Cocaine/*analogs & derivatives/*pharmacology [MESH] |Coronary Vessels/cytology/drug effects [MESH] |Endothelial Cells/*drug effects/metabolism [MESH] |Human Umbilical Vein Endothelial Cells/drug effects/metabolism [MESH] |Humans [MESH] |In Vitro Techniques [MESH] |P-Selectin/*drug effects/metabolism [MESH] |Sensitivity and Specificity [MESH] |Thrombosis/physiopathology [MESH]Cocaine and specific cocaine metabolites induce von Willebrand factor (epmc).pdf DeepDyve Pubget Overpricing