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10.1161/CIRCULATIONAHA.115.020633 http://scihub22266oqcxt.onion/10.1161/CIRCULATIONAHA.115.020633 C4889496!4889496!27154726     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\27154726.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Circulation 2016 ; 133 (22): 2169-79 Nephropedia Template TP {{tp|p=27154726|t=2016. Fpr2/ALX Regulates Neutrophil-Platelet Aggregation and Attenuates Cerebral Inflammation: Impact for Therapy in Cardiovascular Disease |pdf=|usr=}}{{27154726}} gab.com Text Fpr2/ALX Regulates Neutrophil-Platelet Aggregation and Attenuates Cerebral Inflammation: Impact for Therapy in Cardiovascular Disease JO: Circulation http://www.kidney.de/pget.php?&tw=1&pmid=27154726 #FOAvip Background: Platelet activation at sites of vascular injury is essential for hemostasis, but it is also a major pathomechanism underlying ischemic injury. As anti-inflammatory therapies limit thrombosis and anti-thrombotic therapies reduce vascular inflammation, we tested the therapeutic potential of two pro-resolving endogenous mediators: Annexin A1 N-terminal derived peptide (AnxA1Ac2?26) and aspirin (ASA) triggered lipoxin A4 (ATL, 15-epi-lipoxin A4), on the cerebral microcirculation following ischemia-reperfusion (I/R) injury. Furthermore, we tested whether the lipoxin A4 receptor, formyl-peptide receptor 2/3 (Fpr2/3, ortholog to human FPR2/ALX), evoked neuro-protective functions following cerebral I/R injury. Methods and Results: Using intravital microscopy, we found that cerebral I/R injury was accompanied by neutrophil and platelet activation and neutrophil-platelet aggregate (NPA) formation within cerebral microvessels. Moreover, ATL activation of neutrophil Fpr2/3 regulated NPA formation in the brain, and inhibited the reactivity of the cerebral microvasculature. The same results were obtained with AnxA1Ac2?26 administration. Blocking Fpr2/ALX with the antagonist Boc2 reversed this effect, and treatments were ineffective in Fpr2/3 knockout mice, who displayed an exacerbated disease severity, evidenced by increased infarct area, blood brain barrier dysfunction, increased neurological score and elevated levels of cytokines. Furthermore, ASA treatment significantly reduced cerebral leukocyte recruitment, and increased endogenous levels of ATL, effects again mediated by Fpr2/3. Conclusions: In summary, Fpr2/ALX is a therapeutic target for initiating endogenous pro-resolving, anti-inflammatory pathways following cerebral I/R injury. Twit Text FOAVip Fpr2/ALX Regulates Neutrophil-Platelet Aggregation and Attenuates Cerebral Inflammation: Impact for Therapy in Cardiovascular Disease ????Circulation http://www.kidney.de/pget.php?&tw=1&pmid=27154726 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27154726 #FOAvip English Wikipedia <ref>{{Cite pmid|27154726}}</ref> Fpr2/ALX Regulates Neutrophil-Platelet Aggregation and Attenuates Cerebral Inflammation: Impact for Therapy in Cardiovascular Disease #MMPMID27154726 Vital SA; Becker F; Holloway PM; Russell J; Perretti M; Granger DN; Gavins FNE Circulation 2016[May]; 133 (22): 2169-79 PMID27154726show ga Background: Platelet activation at sites of vascular injury is essential for hemostasis, but it is also a major pathomechanism underlying ischemic injury. As anti-inflammatory therapies limit thrombosis and anti-thrombotic therapies reduce vascular inflammation, we tested the therapeutic potential of two pro-resolving endogenous mediators: Annexin A1 N-terminal derived peptide (AnxA1Ac2?26) and aspirin (ASA) triggered lipoxin A4 (ATL, 15-epi-lipoxin A4), on the cerebral microcirculation following ischemia-reperfusion (I/R) injury. Furthermore, we tested whether the lipoxin A4 receptor, formyl-peptide receptor 2/3 (Fpr2/3, ortholog to human FPR2/ALX), evoked neuro-protective functions following cerebral I/R injury. Methods and Results: Using intravital microscopy, we found that cerebral I/R injury was accompanied by neutrophil and platelet activation and neutrophil-platelet aggregate (NPA) formation within cerebral microvessels. Moreover, ATL activation of neutrophil Fpr2/3 regulated NPA formation in the brain, and inhibited the reactivity of the cerebral microvasculature. The same results were obtained with AnxA1Ac2?26 administration. Blocking Fpr2/ALX with the antagonist Boc2 reversed this effect, and treatments were ineffective in Fpr2/3 knockout mice, who displayed an exacerbated disease severity, evidenced by increased infarct area, blood brain barrier dysfunction, increased neurological score and elevated levels of cytokines. Furthermore, ASA treatment significantly reduced cerebral leukocyte recruitment, and increased endogenous levels of ATL, effects again mediated by Fpr2/3. Conclusions: In summary, Fpr2/ALX is a therapeutic target for initiating endogenous pro-resolving, anti-inflammatory pathways following cerebral I/R injury. äFpr2/ALX Regulates Neutrophil-Platelet Aggregation and Attenuates Cere(epmc).pdf DeepDyve Pubget Overpricing