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10.1182/blood-2014-05-573543 http://scihub22266oqcxt.onion/10.1182/blood-2014-05-573543 C4260364!4260364 !25082876     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25082876 &cmd=llinks): Failed to open stream: HTTP request failed! 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Platelets release mitochondria serving as substrate for bactericidal group IIA-secreted phospholipase A2 to promote inflammation |pdf=|usr=}}{{25082876 }} gab.com Text Platelets release mitochondria serving as substrate for bactericidal group IIA-secreted phospholipase A2 to promote inflammation JO: Blood http://www.kidney.de/pget.php?&tw=1&pmid=25082876 #FOAvip Mitochondrial DNA (mtDNA) is a highly potent inflammatory trigger and is reportedly found outside the cells in blood in various pathologies. Platelets are abundant in blood where they promote hemostasis. Although lacking a nucleus, platelets contain functional mitochondria. On activation, platelets produce extracellular vesicles known as microparticles. We hypothesized that activated platelets could also release their mitochondria. We show that activated platelets release respiratory-competent mitochondria, both within membrane-encapsulated microparticles and as free organelles. Extracellular mitochondria are found in platelet concentrates used for transfusion and are present at higher levels in those that induced acute reactions (febrile nonhemolytic reactions, skin manifestations, and cardiovascular events) in transfused patients. We establish that the mitochondrion is an endogenous substrate of secreted phospholipase A2 IIA (sPLA2-IIA), a phospholipase otherwise specific for bacteria, likely reflecting the ancestral proteobacteria origin of mitochondria. The hydrolysis of the mitochondrial membrane by sPLA2-IIA yields inflammatory mediators (ie, lysophospholipids, fatty acids, and mtDNA) that promote leukocyte activation. Two-photon microscopy in live transfused animals revealed that extracellular mitochondria interact with neutrophils in vivo, triggering neutrophil adhesion to the endothelial wall. Our findings identify extracellular mitochondria, produced by platelets, at the midpoint of a potent mechanism leading to inflammatory responses. Twit Text FOAVip Platelets release mitochondria serving as substrate for bactericidal group IIA-secreted phospholipase A2 to promote inflammation ????Blood http://www.kidney.de/pget.php?&tw=1&pmid=25082876 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25082876 #FOAvip English Wikipedia <ref>{{Cite pmid|25082876 }}</ref> Platelets release mitochondria serving as substrate for bactericidal group IIA-secreted phospholipase A2 to promote inflammation #MMPMID25082876 Boudreau LH ; Duchez AC ; Cloutier N ; Soulet D ; Martin N ; Bollinger J ; Paré A ; Rousseau M ; Naika GS ; Lévesque T ; Laflamme C ; Marcoux G ; Lambeau G ; Farndale RW ; Pouliot M ; Hamzeh-Cognasse H ; Cognasse F ; Garraud O ; Nigrovic PA ; Guderley H ; Lacroix S ; Thibault L ; Semple JW ; Gelb MH ; Boilard E Blood 2014[Oct]; 124 (14 ): 2173-83 PMID25082876 show ga Mitochondrial DNA (mtDNA) is a highly potent inflammatory trigger and is reportedly found outside the cells in blood in various pathologies. Platelets are abundant in blood where they promote hemostasis. Although lacking a nucleus, platelets contain functional mitochondria. On activation, platelets produce extracellular vesicles known as microparticles. We hypothesized that activated platelets could also release their mitochondria. We show that activated platelets release respiratory-competent mitochondria, both within membrane-encapsulated microparticles and as free organelles. Extracellular mitochondria are found in platelet concentrates used for transfusion and are present at higher levels in those that induced acute reactions (febrile nonhemolytic reactions, skin manifestations, and cardiovascular events) in transfused patients. We establish that the mitochondrion is an endogenous substrate of secreted phospholipase A2 IIA (sPLA2-IIA), a phospholipase otherwise specific for bacteria, likely reflecting the ancestral proteobacteria origin of mitochondria. The hydrolysis of the mitochondrial membrane by sPLA2-IIA yields inflammatory mediators (ie, lysophospholipids, fatty acids, and mtDNA) that promote leukocyte activation. Two-photon microscopy in live transfused animals revealed that extracellular mitochondria interact with neutrophils in vivo, triggering neutrophil adhesion to the endothelial wall. Our findings identify extracellular mitochondria, produced by platelets, at the midpoint of a potent mechanism leading to inflammatory responses. |Animals [MESH] |Blood Platelets/*metabolism [MESH] |DNA, Mitochondrial/metabolism [MESH] |Endothelium, Vascular/metabolism [MESH] |Flow Cytometry [MESH] |Group II Phospholipases A2/*metabolism [MESH] |Humans [MESH] |Inflammation/*metabolism [MESH] |Male [MESH] |Mice [MESH] |Mice, Inbred C57BL [MESH] |Mitochondria/*metabolism [MESH] |Platelet Activation [MESH]Platelets release mitochondria serving as substrate for bactericidal g(epmc).pdf DeepDyve Pubget Overpricing