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10.1161/ATVBAHA.111.227116 http://scihub22266oqcxt.onion/10.1161/ATVBAHA.111.227116 C4909471!4909471 !21817096     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=21817096 &cmd=llinks): Failed to open stream: HTTP request failed! 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Human neutrophil peptides mediate endothelial-monocyte interaction, foam cell formation, and platelet activation |pdf=|usr=}}{{21817096 }} gab.com Text Human neutrophil peptides mediate endothelial-monocyte interaction, foam cell formation, and platelet activation JO: Arterioscler Thromb Vasc Biol http://www.kidney.de/pget.php?&tw=1&pmid=21817096 #FOAvip OBJECTIVE: Neutrophils are involved in the inflammatory responses during atherosclerosis. Human neutrophil peptides (HNPs) released from activated neutrophils exert immune modulating properties. We hypothesized that HNPs play an important role in neutrophil-mediated inflammatory cardiovascular responses in atherosclerosis. METHODS AND RESULTS: We examined the role of HNPs in endothelial-leukocyte interaction, platelet activation, and foam cell formation in vitro and in vivo. We demonstrated that stimulation of human coronary artery endothelial cells with clinically relevant concentrations of HNPs resulted in monocyte adhesion and transmigration; induction of oxidative stress in human macrophages, which accelerates foam cell formation; and activation and aggregation of human platelets. The administration of superoxide dismutase or anti-CD36 antibody reduced foam cell formation and cholesterol efflux. Mice deficient in double genes of low-density lipoprotein receptor and low-density lipoprotein receptor-related protein (LRP), and mice deficient in a single gene of LRP8, the only LRP phenotype expressed in platelets, showed reduced leukocyte rolling and decreased platelet aggregation and thrombus formation in response to HNP stimulation. CONCLUSIONS: HNPs exert proatherosclerotic properties that appear to be mediated through LRP8 signaling pathways, suggesting an important role for HNPs in the development of inflammatory cardiovascular diseases. Twit Text FOAVip Human neutrophil peptides mediate endothelial-monocyte interaction, foam cell formation, and platelet activation ????Arterioscler Thromb Vasc Biol http://www.kidney.de/pget.php?&tw=1&pmid=21817096 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=21817096 #FOAvip English Wikipedia <ref>{{Cite pmid|21817096 }}</ref> Human neutrophil peptides mediate endothelial-monocyte interaction, foam cell formation, and platelet activation #MMPMID21817096 Quinn KL ; Henriques M ; Tabuchi A ; Han B ; Yang H ; Cheng WE ; Tole S ; Yu H ; Luo A ; Charbonney E ; Tullis E ; Lazarus A ; Robinson LA ; Ni H ; Peterson BR ; Kuebler WM ; Slutsky AS ; Zhang H Arterioscler Thromb Vasc Biol 2011[Sep]; 31 (9 ): 2070-9 PMID21817096 show ga OBJECTIVE: Neutrophils are involved in the inflammatory responses during atherosclerosis. Human neutrophil peptides (HNPs) released from activated neutrophils exert immune modulating properties. We hypothesized that HNPs play an important role in neutrophil-mediated inflammatory cardiovascular responses in atherosclerosis. METHODS AND RESULTS: We examined the role of HNPs in endothelial-leukocyte interaction, platelet activation, and foam cell formation in vitro and in vivo. We demonstrated that stimulation of human coronary artery endothelial cells with clinically relevant concentrations of HNPs resulted in monocyte adhesion and transmigration; induction of oxidative stress in human macrophages, which accelerates foam cell formation; and activation and aggregation of human platelets. The administration of superoxide dismutase or anti-CD36 antibody reduced foam cell formation and cholesterol efflux. Mice deficient in double genes of low-density lipoprotein receptor and low-density lipoprotein receptor-related protein (LRP), and mice deficient in a single gene of LRP8, the only LRP phenotype expressed in platelets, showed reduced leukocyte rolling and decreased platelet aggregation and thrombus formation in response to HNP stimulation. CONCLUSIONS: HNPs exert proatherosclerotic properties that appear to be mediated through LRP8 signaling pathways, suggesting an important role for HNPs in the development of inflammatory cardiovascular diseases. |*Cell Communication [MESH] |*Platelet Activation [MESH] |Animals [MESH] |Atherosclerosis/etiology [MESH] |Chemokines/biosynthesis [MESH] |Endothelial Cells/*physiology [MESH] |Foam Cells/*physiology [MESH] |Humans [MESH] |LDL-Receptor Related Proteins/physiology [MESH] |Low Density Lipoprotein Receptor-Related Protein-1/physiology [MESH] |Male [MESH] |Mice [MESH] |Monocytes/*physiology [MESH] |Neutrophil Activation [MESH] |Oxidative Stress [MESH] |Platelet Aggregation [MESH]Human neutrophil peptides mediate endothelial-monocyte interaction, fo(epmc).pdf DeepDyve Pubget Overpricing