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10.1074/jbc.M116.768309 http://scihub22266oqcxt.onion/10.1074/jbc.M116.768309 C5448091!5448091 !28408624     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28408624 &cmd=llinks): Failed to open stream: HTTP request failed! 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Activated protein C inhibits neutrophil extracellular trap formation in vitro and activation in vivo |pdf=|usr=}}{{28408624 }} gab.com Text Activated protein C inhibits neutrophil extracellular trap formation in vitro and activation in vivo JO: J Biol Chem http://www.kidney.de/pget.php?&tw=1&pmid=28408624 #FOAvip Activated protein C (APC) is a multifunctional serine protease with anticoagulant, cytoprotective, and anti-inflammatory activities. In addition to the cytoprotective effects of APC on endothelial cells, podocytes, and neurons, APC cleaves and detoxifies extracellular histones, a major component of neutrophil extracellular traps (NETs). NETs promote pathogen clearance but also can lead to thrombosis; the pathways that negatively regulate NETosis are largely unknown. Thus, we studied whether APC is capable of directly inhibiting NETosis via receptor-mediated cell signaling mechanisms. Here, by quantifying extracellular DNA or myeloperoxidase, we demonstrate that APC binds human leukocytes and prevents activated platelet supernatant or phorbol 12-myristate 13-acetate (PMA) from inducing NETosis. Of note, APC proteolytic activity was required for inhibiting NETosis. Moreover, antibodies against the neutrophil receptors endothelial protein C receptor (EPCR), protease-activated receptor 3 (PAR3), and macrophage-1 antigen (Mac-1) blocked APC inhibition of NETosis. Select mutations in the Gla and protease domains of recombinant APC caused a loss of NETosis. Interestingly, pretreatment of neutrophils with APC prior to induction of NETosis inhibited platelet adhesion to NETs. Lastly, in a nonhuman primate model of Escherichia coli-induced sepsis, pretreatment of animals with APC abrogated release of myeloperoxidase from neutrophils, a marker of neutrophil activation. These findings suggest that the anti-inflammatory function of APC at therapeutic concentrations may include the inhibition of NETosis in an EPCR-, PAR3-, and Mac-1-dependent manner, providing additional mechanistic insight into the diverse functions of neutrophils and APC in disease states including sepsis. Twit Text FOAVip Activated protein C inhibits neutrophil extracellular trap formation in vitro and activation in vivo ????J Biol Chem http://www.kidney.de/pget.php?&tw=1&pmid=28408624 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28408624 #FOAvip English Wikipedia <ref>{{Cite pmid|28408624 }}</ref> Activated protein C inhibits neutrophil extracellular trap formation in vitro and activation in vivo #MMPMID28408624 Healy LD ; Puy C ; Fernández JA ; Mitrugno A ; Keshari RS ; Taku NA ; Chu TT ; Xu X ; Gruber A ; Lupu F ; Griffin JH ; McCarty OJT J Biol Chem 2017[May]; 292 (21 ): 8616-8629 PMID28408624 show ga Activated protein C (APC) is a multifunctional serine protease with anticoagulant, cytoprotective, and anti-inflammatory activities. In addition to the cytoprotective effects of APC on endothelial cells, podocytes, and neurons, APC cleaves and detoxifies extracellular histones, a major component of neutrophil extracellular traps (NETs). NETs promote pathogen clearance but also can lead to thrombosis; the pathways that negatively regulate NETosis are largely unknown. Thus, we studied whether APC is capable of directly inhibiting NETosis via receptor-mediated cell signaling mechanisms. Here, by quantifying extracellular DNA or myeloperoxidase, we demonstrate that APC binds human leukocytes and prevents activated platelet supernatant or phorbol 12-myristate 13-acetate (PMA) from inducing NETosis. Of note, APC proteolytic activity was required for inhibiting NETosis. Moreover, antibodies against the neutrophil receptors endothelial protein C receptor (EPCR), protease-activated receptor 3 (PAR3), and macrophage-1 antigen (Mac-1) blocked APC inhibition of NETosis. Select mutations in the Gla and protease domains of recombinant APC caused a loss of NETosis. Interestingly, pretreatment of neutrophils with APC prior to induction of NETosis inhibited platelet adhesion to NETs. Lastly, in a nonhuman primate model of Escherichia coli-induced sepsis, pretreatment of animals with APC abrogated release of myeloperoxidase from neutrophils, a marker of neutrophil activation. These findings suggest that the anti-inflammatory function of APC at therapeutic concentrations may include the inhibition of NETosis in an EPCR-, PAR3-, and Mac-1-dependent manner, providing additional mechanistic insight into the diverse functions of neutrophils and APC in disease states including sepsis. |Animals [MESH] |Antigens, CD/immunology/metabolism [MESH] |Disease Models, Animal [MESH] |Endothelial Protein C Receptor [MESH] |Escherichia coli [MESH] |Escherichia coli Infections/blood/immunology [MESH] |Extracellular Traps/*immunology/metabolism [MESH] |Female [MESH] |Humans [MESH] |Macrophage-1 Antigen/immunology/metabolism [MESH] |Male [MESH] |Neutrophil Activation/drug effects/*immunology [MESH] |Neutrophils/*immunology/metabolism [MESH] |Papio anubis [MESH] |Protein C/*immunology/metabolism [MESH] |Receptors, Cell Surface/immunology/metabolism [MESH] |Sepsis/blood/immunology [MESH]Activated protein C inhibits neutrophil extracellular trap formation i(epmc).pdf DeepDyve Pubget Overpricing