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10.4049/jimmunol.1201487 http://scihub22266oqcxt.onion/10.4049/jimmunol.1201487 C4485405!4485405!23105142     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 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 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 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Immunol 2012 ; 189 (11): 5411-20 Nephropedia Template TP {{tp|p=23105142|t=2012. Endothelial Cell Peroxisome Proliferator-activated Receptor ? Reduces Endotoxemic Pulmonary Inflammation and Injury |pdf=|usr=}}{{23105142}} gab.com Text Endothelial Cell Peroxisome Proliferator-activated Receptor Reduces Endotoxemic Pulmonary Inflammation and Injury JO: J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=23105142 #FOAvip Bacterial endotoxin (LPS)-mediated sepsis involves severe, dysregulated inflammation that injures the lungs and other organs, often fatally. Vascular endothelial cells are both key mediators and targets of LPS-induced inflammatory responses. The nuclear hormone receptor peroxisome proliferator-activated receptor ? (PPAR?) exerts anti-inflammatory actions in various cells, but it is unknown whether it modulates inflammation through actions within endothelial cells. To determine whether PPAR? acts within endothelial cells to diminish endotoxemic lung inflammation and injury, we measured inflammatory responses and mediators in mice with endothelial-targeted deletion of PPAR?. Endothelial cell PPAR? (ePPAR?) knockout exacerbated LPS-induced pulmonary inflammation and injury as shown by several measures, including infiltration of inflammatory cells, edema, and production of reactive oxygen species and pro-inflammatory cytokines, along with upregulation of the LPS receptor TLR4 in lung tissue and increased activation of its downstream signaling pathways. In isolated LPS-stimulated endothelial cells in vitro, absence of PPAR? enhanced the production of numerous inflammatory markers. We hypothesized that the observed in vivo activity of the ligand-activated ePPAR? may arise in part from nitrated fatty acids (NFAs), a novel class of endogenous PPAR? ligands. Supporting this idea, we found that treating isolated endothelial cells with physiologically relevant concentrations of the endogenous NFA 10-nitro-oleate reduced LPS-induced expression of a wide range of inflammatory markers in the presence of PPAR?, but not in its absence, and also inhibited neutrophil mobility in a PPAR??dependent manner. Our results demonstrate a key protective role of ePPAR? against endotoxemic injury, and a potential ePPAR??mediated anti-inflammatory role for NFAs. Twit Text FOAVip Endothelial Cell Peroxisome Proliferator-activated Receptor Reduces Endotoxemic Pulmonary Inflammation and Injury ????J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=23105142 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=23105142 #FOAvip English Wikipedia <ref>{{Cite pmid|23105142}}</ref> Endothelial Cell Peroxisome Proliferator-activated Receptor ? Reduces Endotoxemic Pulmonary Inflammation and Injury #MMPMID23105142 Reddy AT; Lakshmi SP; Kleinhenz JM; Sutliff RL; Hart CM; Reddy RC J Immunol 2012[Dec]; 189 (11): 5411-20 PMID23105142show ga Bacterial endotoxin (LPS)-mediated sepsis involves severe, dysregulated inflammation that injures the lungs and other organs, often fatally. Vascular endothelial cells are both key mediators and targets of LPS-induced inflammatory responses. The nuclear hormone receptor peroxisome proliferator-activated receptor ? (PPAR?) exerts anti-inflammatory actions in various cells, but it is unknown whether it modulates inflammation through actions within endothelial cells. To determine whether PPAR? acts within endothelial cells to diminish endotoxemic lung inflammation and injury, we measured inflammatory responses and mediators in mice with endothelial-targeted deletion of PPAR?. Endothelial cell PPAR? (ePPAR?) knockout exacerbated LPS-induced pulmonary inflammation and injury as shown by several measures, including infiltration of inflammatory cells, edema, and production of reactive oxygen species and pro-inflammatory cytokines, along with upregulation of the LPS receptor TLR4 in lung tissue and increased activation of its downstream signaling pathways. In isolated LPS-stimulated endothelial cells in vitro, absence of PPAR? enhanced the production of numerous inflammatory markers. We hypothesized that the observed in vivo activity of the ligand-activated ePPAR? may arise in part from nitrated fatty acids (NFAs), a novel class of endogenous PPAR? ligands. Supporting this idea, we found that treating isolated endothelial cells with physiologically relevant concentrations of the endogenous NFA 10-nitro-oleate reduced LPS-induced expression of a wide range of inflammatory markers in the presence of PPAR?, but not in its absence, and also inhibited neutrophil mobility in a PPAR??dependent manner. Our results demonstrate a key protective role of ePPAR? against endotoxemic injury, and a potential ePPAR??mediated anti-inflammatory role for NFAs. äEndothelial Cell Peroxisome Proliferator-activated Receptor ? Reduces (epmc).pdf DeepDyve Pubget Overpricing