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10.1111/bph.12768 http://scihub22266oqcxt.onion/10.1111/bph.12768 C4243981!4243981!24824742     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 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 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       Br+J+Pharmacol 2014 ; 171 (17): 4087-96 Nephropedia Template TP {{tp|p=24824742|t=2014. A formyl peptide receptor agonist suppresses inflammation and bone damage in arthritis |pdf=|usr=}}{{24824742}} gab.com Text A formyl peptide receptor agonist suppresses inflammation and bone damage in arthritis JO: Br J Pharmacol http://www.kidney.de/pget.php?&tw=1&pmid=24824742 #FOAvip Background and Purpose: Annexin A1 (AnxA1) is an endogenous anti-inflammatory protein and agonist of the formyl peptide receptor 2 (FPR2). However, the potential for therapeutic FPR ligands to modify immune-mediated disease has been little explored. We investigated the effects of a synthetic FPR agonist on joint disease in the K/BxN model of rheumatoid arthritis (RA) and RA fibroblast-like synoviocytes (FLS). Experimental Approach: Arthritis was induced by injection of K/BxN serum at day 0 and 2 in wild-type (WT) or AnxA1?/? mice and clinical and histopathological manifestations measured 8?11 days later. WT mice were given the FPR agonist compound 43 (Cpd43) (6 or 30?mg·kg?1 i.p.) for 4 days. Effects of AnxA1 and Cpd43 on RANKL-induced osteoclastogenesis were assessed in RAW 264.7 cells and human RA FLS and macrophages. Key Results: Treatment with Cpd43 before or after the onset of arthritis reduced clinical disease severity and attenuated synovial TNF-? and osteoclast-associated gene expression. Deletion of AnxA1 in mice exacerbated arthritis severity in the K/BxN model. In vitro, Cpd43 suppressed osteoclastogenesis and NFAT activity elicited by RANKL, and inhibited IL-6 secretion by mouse macrophages. In human RA joint-derived FLS and monocyte-derived macrophages, Cpd43 treatment inhibited IL-6 release, while blocking FPR2 or silencing AnxA1 increased this release. Conclusions and Implications: The FPR agonist Cpd43 reduced osteoclastogenesis and inflammation in a mouse model of RA and exhibited anti-inflammatory effects in relevant human cells. These data suggest that FPR ligands may represent novel therapeutic agents capable of ameliorating inflammation and bone damage in RA. Twit Text FOAVip A formyl peptide receptor agonist suppresses inflammation and bone damage in arthritis ????Br J Pharmacol http://www.kidney.de/pget.php?&tw=1&pmid=24824742 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24824742 #FOAvip English Wikipedia <ref>{{Cite pmid|24824742}}</ref> A formyl peptide receptor agonist suppresses inflammation and bone damage in arthritis #MMPMID24824742 Kao W; Gu R; Jia Y; Wei X; Fan H; Harris J; Zhang Z; Quinn J; Morand EF; Yang YH Br J Pharmacol 2014[Sep]; 171 (17): 4087-96 PMID24824742show ga Background and Purpose: Annexin A1 (AnxA1) is an endogenous anti-inflammatory protein and agonist of the formyl peptide receptor 2 (FPR2). However, the potential for therapeutic FPR ligands to modify immune-mediated disease has been little explored. We investigated the effects of a synthetic FPR agonist on joint disease in the K/BxN model of rheumatoid arthritis (RA) and RA fibroblast-like synoviocytes (FLS). Experimental Approach: Arthritis was induced by injection of K/BxN serum at day 0 and 2 in wild-type (WT) or AnxA1?/? mice and clinical and histopathological manifestations measured 8?11 days later. WT mice were given the FPR agonist compound 43 (Cpd43) (6 or 30?mg·kg?1 i.p.) for 4 days. Effects of AnxA1 and Cpd43 on RANKL-induced osteoclastogenesis were assessed in RAW 264.7 cells and human RA FLS and macrophages. Key Results: Treatment with Cpd43 before or after the onset of arthritis reduced clinical disease severity and attenuated synovial TNF-? and osteoclast-associated gene expression. Deletion of AnxA1 in mice exacerbated arthritis severity in the K/BxN model. In vitro, Cpd43 suppressed osteoclastogenesis and NFAT activity elicited by RANKL, and inhibited IL-6 secretion by mouse macrophages. In human RA joint-derived FLS and monocyte-derived macrophages, Cpd43 treatment inhibited IL-6 release, while blocking FPR2 or silencing AnxA1 increased this release. Conclusions and Implications: The FPR agonist Cpd43 reduced osteoclastogenesis and inflammation in a mouse model of RA and exhibited anti-inflammatory effects in relevant human cells. These data suggest that FPR ligands may represent novel therapeutic agents capable of ameliorating inflammation and bone damage in RA. äA formyl peptide receptor agonist suppresses inflammation and bone dam(epmc).pdf DeepDyve Pubget Overpricing