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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 Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28955836 &cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 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 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\28955836 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Biochem+Biophys+Rep 2016 ; 5 (ä): 290-295 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): 290-295 PMID28955836 show 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