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10.1016/j.bbrep.2016.01.009 http://scihub22266oqcxt.onion/10.1016/j.bbrep.2016.01.009 C5600337!5600337!28955836     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       Biochem+Biophys+Rep 2016 ; 5 (ä): 290-5 Nephropedia Template TP {{tp|p=28955836|t=2016. Pentraxin-3 regulates the inflammatory activity of macrophages |pdf=|usr=}}{{28955836}} gab.com Text Pentraxin-3 regulates the inflammatory activity of macrophages JO: Biochem Biophys Rep http://www.kidney.de/pget.php?&tw=1&pmid=28955836 #FOAvip Background and aims: Pentraxin-3 (PTX3) reportedly has protective roles in atherosclerosis and myocardial infarction, and is a useful biomarker of vascular inflammation. However, the detailed functions of PTX3 in inflammation are yet to be elucidated. This study aimed to investigate the function of PTX3 in macrophages. Methods: PMA-treated THP-1 cell line (THP-1 macrophage) and monocyte-derived human primary macrophages were treated with recombinant PTX3. Cytokine and chemokine levels in the THP-1 culture medium were measured as well as monocyte chemoattractant protein (MCP-1) concentrations in the Raw 264.7 cell culture medium. PTX3-silenced apoptotic macrophages (THP-1 cell line) were generated to investigate the roles of PTX3 in phagocytosis. Results: In the presence of PTX3, macrophage interleukin-1? (IL-1?), tumor necrosis factor-alpha (TNF-?) and MCP-1 levels were reduced significantly (?39%, P=0.007; ?21%, P=0.008; and ?67%, P=0.0003, respectively), whilst activated transforming growth factor-? (TGF??) was detected in the THP-1 macrophages (P=0.0004). Additionally, PTX3 induced Akt phosphorylation and reduced nuclear factor-kappa B (NF-?B) activation by 35% (P=0.002), which was induced by TNF-? in THP-1 macrophages. Furthermore, silencing of PTX3 in apoptotic cells resulted in increased macrophage binding, elevated expression rate of HLA-DR (+30%, P=0.015) and CD86 (+204%, P=0.004) positive cells, and induction of IL-1? (+36%, P=0.024) production. Conversely, adding recombinant PTX3 to macrophages reduced CD86 and HLA-DR expression in a dose-dependent manner. Conclusions: We identified PTX3 as a novel regulator of macrophage activity, and this function suggests that PTX3 acts to resolve inflammation. Twit Text FOAVip Pentraxin-3 regulates the inflammatory activity of macrophages ????Biochem Biophys Rep http://www.kidney.de/pget.php?&tw=1&pmid=28955836 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28955836 #FOAvip English Wikipedia <ref>{{Cite pmid|28955836}}</ref> Pentraxin-3 regulates the inflammatory activity of macrophages #MMPMID28955836 Shiraki A; Kotooka N; Komoda H; Hirase T; Oyama Ji; Node K Biochem Biophys Rep 2016[Mar]; 5 (ä): 290-5 PMID28955836show ga Background and aims: Pentraxin-3 (PTX3) reportedly has protective roles in atherosclerosis and myocardial infarction, and is a useful biomarker of vascular inflammation. However, the detailed functions of PTX3 in inflammation are yet to be elucidated. This study aimed to investigate the function of PTX3 in macrophages. Methods: PMA-treated THP-1 cell line (THP-1 macrophage) and monocyte-derived human primary macrophages were treated with recombinant PTX3. Cytokine and chemokine levels in the THP-1 culture medium were measured as well as monocyte chemoattractant protein (MCP-1) concentrations in the Raw 264.7 cell culture medium. PTX3-silenced apoptotic macrophages (THP-1 cell line) were generated to investigate the roles of PTX3 in phagocytosis. Results: In the presence of PTX3, macrophage interleukin-1? (IL-1?), tumor necrosis factor-alpha (TNF-?) and MCP-1 levels were reduced significantly (?39%, P=0.007; ?21%, P=0.008; and ?67%, P=0.0003, respectively), whilst activated transforming growth factor-? (TGF??) was detected in the THP-1 macrophages (P=0.0004). Additionally, PTX3 induced Akt phosphorylation and reduced nuclear factor-kappa B (NF-?B) activation by 35% (P=0.002), which was induced by TNF-? in THP-1 macrophages. Furthermore, silencing of PTX3 in apoptotic cells resulted in increased macrophage binding, elevated expression rate of HLA-DR (+30%, P=0.015) and CD86 (+204%, P=0.004) positive cells, and induction of IL-1? (+36%, P=0.024) production. Conversely, adding recombinant PTX3 to macrophages reduced CD86 and HLA-DR expression in a dose-dependent manner. Conclusions: We identified PTX3 as a novel regulator of macrophage activity, and this function suggests that PTX3 acts to resolve inflammation. äPentraxin-3 regulates the inflammatory activity of macrophages (epmc).pdf DeepDyve Pubget Overpricing