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10.1111/jth.13620 http://scihub22266oqcxt.onion/10.1111/jth.13620 C5378657!5378657!28079976     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Thromb+Haemost 2017 ; 15 (4): 802-13 Nephropedia Template TP {{tp|p=28079976|t=2017. Maresin 1 induces a novel pro-resolving phenotype in human platelets |pdf=|usr=}}{{28079976}} gab.com Text Maresin 1 induces a novel pro-resolving phenotype in human platelets JO: J Thromb Haemost http://www.kidney.de/pget.php?&tw=1&pmid=28079976 #FOAvip Background: Antiplatelet therapy is a cornerstone of modern medical practice and is routinely employed to reduce the likelihood of myocardial infarction, thrombosis, and stroke. However, current antiplatelet therapies, such as aspirin, often have adverse side effects, including increased risk of bleeding, and some patients are relatively ?aspirin-resistant?. Platelets are intimately involved in hemostasis and inflammation, and clinical consequences are associated with excessive or insufficient platelet activation. Objectives: A major unmet need in the field of hematology is the development of new agents that safely prevent unwanted platelet activation in patients with underlying cardiovascular disease, while minimizing the risk of bleeding. Here, we investigate the potential of endogenously produced, specialized pro-resolving mediators (SPMs) as novel antiplatelet agents. SPMs are a recently discovered class of lipid-derived molecules that drive the resolution of inflammation, without being overtly immunosuppressive. Methods: Human platelets were treated with lipoxin A4, resolvin D1, resolvin D2, 17-HDHA, or maresin 1 for 15 minutes, then were subjected to platelet function tests, including spreading, aggregation, and inflammatory mediator release. Results: We show for the first time that human platelets express the SPM receptors, GPR32 and ALX. Furthermore, our data demonstrate that maresin 1 differentially regulates platelet hemostatic function, by enhancing platelet aggregation and spreading, while suppressing release of proinflammatory and pro-thrombotic mediators. Conclusions: These data support the concept that SPMs differentially regulate platelet function and may represent a novel class of antiplatelet agents. SPMs also may play an important role in the resolution of inflammation in cardiovascular diseases. Twit Text FOAVip Maresin 1 induces a novel pro-resolving phenotype in human platelets ????J Thromb Haemost http://www.kidney.de/pget.php?&tw=1&pmid=28079976 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28079976 #FOAvip English Wikipedia <ref>{{Cite pmid|28079976}}</ref> Maresin 1 induces a novel pro-resolving phenotype in human platelets #MMPMID28079976 Lannan KL; Spinelli SL; Blumberg N; Phipps RP J Thromb Haemost 2017[Apr]; 15 (4): 802-13 PMID28079976show ga Background: Antiplatelet therapy is a cornerstone of modern medical practice and is routinely employed to reduce the likelihood of myocardial infarction, thrombosis, and stroke. However, current antiplatelet therapies, such as aspirin, often have adverse side effects, including increased risk of bleeding, and some patients are relatively ?aspirin-resistant?. Platelets are intimately involved in hemostasis and inflammation, and clinical consequences are associated with excessive or insufficient platelet activation. Objectives: A major unmet need in the field of hematology is the development of new agents that safely prevent unwanted platelet activation in patients with underlying cardiovascular disease, while minimizing the risk of bleeding. Here, we investigate the potential of endogenously produced, specialized pro-resolving mediators (SPMs) as novel antiplatelet agents. SPMs are a recently discovered class of lipid-derived molecules that drive the resolution of inflammation, without being overtly immunosuppressive. Methods: Human platelets were treated with lipoxin A4, resolvin D1, resolvin D2, 17-HDHA, or maresin 1 for 15 minutes, then were subjected to platelet function tests, including spreading, aggregation, and inflammatory mediator release. Results: We show for the first time that human platelets express the SPM receptors, GPR32 and ALX. Furthermore, our data demonstrate that maresin 1 differentially regulates platelet hemostatic function, by enhancing platelet aggregation and spreading, while suppressing release of proinflammatory and pro-thrombotic mediators. Conclusions: These data support the concept that SPMs differentially regulate platelet function and may represent a novel class of antiplatelet agents. SPMs also may play an important role in the resolution of inflammation in cardiovascular diseases. äMaresin 1 induces a novel pro-resolving phenotype in human platelets (epmc).pdf DeepDyve Pubget Overpricing