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10.4049/jimmunol.1700315 http://scihub22266oqcxt.onion/10.4049/jimmunol.1700315 C5583748!5583748 !28794232     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 298.79999999999995 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 298.79999999999995 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 298.79999999999995 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 298.79999999999995 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\28794232 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       J+Immunol 2017 ; 199 (6 ): 2043-2054 Nephropedia Template TP {{tp|p=28794232 |t=2017. Resolvin D1 Improves the Resolution of Inflammation via Activating NF-?B p50/p50-Mediated Cyclooxygenase-2 Expression in Acute Respiratory Distress Syndrome |pdf=|usr=}}{{28794232 }} gab.com Text Resolvin D1 Improves the Resolution of Inflammation via Activating NF- B p50/p50-Mediated Cyclooxygenase-2 Expression in Acute Respiratory Distress Syndrome JO: J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=28794232 #FOAvip Acute respiratory distress syndrome (ARDS) is a severe illness characterized by uncontrolled inflammation. The resolution of inflammation is a tightly regulated event controlled by endogenous mediators, such as resolvin D1 (RvD1). Cyclooxygenase-2 (COX-2) has been reported to promote inflammation, along with PGE(2), in the initiation of inflammation, as well as in prompting resolution, with PGD(2) acting in the later phase of inflammation. Our previous work demonstrated that RvD1 enhanced COX-2 and PGD(2) expression to resolve inflammation. In this study, we investigated mechanisms underlying the effect of RvD1 in modulating proresolving COX-2 expression. In a self-limited ARDS model, an LPS challenge induced the biphasic activation of COX-2, and RvD1 promoted COX-2 expression during the resolution phase. However, it was significantly blocked by treatment of a NF-?B inhibitor. In pulmonary fibroblasts, NF-?B p50/p50 was shown to be responsible for the proresolving activity of COX-2. Additionally, RvD1 potently promoted p50 homodimer nuclear translocation and robustly triggered DNA-binding activity, upregulating COX-2 expression via lipoxin A(4) receptor/formyl peptide receptor 2. Finally, the absence of p50 in knockout mice prevented RvD1 from promoting COX-2 and PGD(2) expression and resulted in excessive pulmonary inflammation. In conclusion, RvD1 expedites the resolution of inflammation through activation of lipoxin A(4) receptor/formyl peptide receptor 2 receptor and NF-?B p50/p50-COX-2 signaling pathways, indicating that RvD1 might have therapeutic potential in the management of ARDS. Twit Text FOAVip Resolvin D1 Improves the Resolution of Inflammation via Activating NF- B p50/p50-Mediated Cyclooxygenase-2 Expression in Acute Respiratory Distress Syndrome ????J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=28794232 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28794232 #FOAvip English Wikipedia <ref>{{Cite pmid|28794232 }}</ref> Resolvin D1 Improves the Resolution of Inflammation via Activating NF-?B p50/p50-Mediated Cyclooxygenase-2 Expression in Acute Respiratory Distress Syndrome #MMPMID28794232 Gao Y ; Zhang H ; Luo L ; Lin J ; Li D ; Zheng S ; Huang H ; Yan S ; Yang J ; Hao Y ; Li H ; Gao Smith F ; Jin S J Immunol 2017[Sep]; 199 (6 ): 2043-2054 PMID28794232 show ga Acute respiratory distress syndrome (ARDS) is a severe illness characterized by uncontrolled inflammation. The resolution of inflammation is a tightly regulated event controlled by endogenous mediators, such as resolvin D1 (RvD1). Cyclooxygenase-2 (COX-2) has been reported to promote inflammation, along with PGE(2), in the initiation of inflammation, as well as in prompting resolution, with PGD(2) acting in the later phase of inflammation. Our previous work demonstrated that RvD1 enhanced COX-2 and PGD(2) expression to resolve inflammation. In this study, we investigated mechanisms underlying the effect of RvD1 in modulating proresolving COX-2 expression. In a self-limited ARDS model, an LPS challenge induced the biphasic activation of COX-2, and RvD1 promoted COX-2 expression during the resolution phase. However, it was significantly blocked by treatment of a NF-?B inhibitor. In pulmonary fibroblasts, NF-?B p50/p50 was shown to be responsible for the proresolving activity of COX-2. Additionally, RvD1 potently promoted p50 homodimer nuclear translocation and robustly triggered DNA-binding activity, upregulating COX-2 expression via lipoxin A(4) receptor/formyl peptide receptor 2. Finally, the absence of p50 in knockout mice prevented RvD1 from promoting COX-2 and PGD(2) expression and resulted in excessive pulmonary inflammation. In conclusion, RvD1 expedites the resolution of inflammation through activation of lipoxin A(4) receptor/formyl peptide receptor 2 receptor and NF-?B p50/p50-COX-2 signaling pathways, indicating that RvD1 might have therapeutic potential in the management of ARDS. äResolvin D1 Improves the Resolution of Inflammation via Activating NF-(epmc).pdf DeepDyve Pubget Overpricing