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10.1016/j.bbagen.2016.07.010 http://scihub22266oqcxt.onion/10.1016/j.bbagen.2016.07.010 C5010974!5010974!27431604     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       Biochim+Biophys+Acta 2016 ; 1860 (11 Pt A): 2428-37 Nephropedia Template TP {{tp|p=27431604|t=2016. NITRO-OLEIC ACID INHIBITS VASCULAR ENDOTHELIAL INFLAMMATORY RESPONSES AND THE ENDOTHELIAL-MESENCHYMAL TRANSITION |pdf=|usr=}}{{27431604}} gab.com Text NITRO-OLEIC ACID INHIBITS VASCULAR ENDOTHELIAL INFLAMMATORY RESPONSES AND THE ENDOTHELIAL-MESENCHYMAL TRANSITION JO: Biochim Biophys Acta http://www.kidney.de/pget.php?&tw=1&pmid=27431604 #FOAvip Background: Inflammatory-mediated pathological processes in the endothelium arise as a consequence of the dysregulation of vascular homeostasis. Of particular importance are mediators produced by stimulated monocytes/macrophages inducing activation of endothelial cells (ECs). This is manifested by excessive soluble pro-inflammatory mediator production and cell surface adhesion molecule expression. Nitro-fatty acids are endogenous products of metabolic and inflammatory reactions that display immuno-regulatory potential and may represent a novel therapeutic strategy to treat inflammatory diseases. The purpose of our study was to characterize the effects of nitro-oleic acid (OA-NO2) on inflammatory responses and the endothelial-mesenchymal transition (EndMT) in ECs that is a consequence of the altered healing phase of the immune response. Methods: The effect of OA-NO2 on inflammatory responses and EndMT was determined in murine macrophages and murine and human ECs using Western blotting, ELISA, immunostaining, and functional assays. Results: OA-NO2 limited the activation of macrophages and ECs by reducing pro-inflammatory cytokine production and adhesion molecule expression through its modulation of STAT, MAPK and NF-?B-regulated signaling. OA-NO2 also decreased transforming growth factor-?-stimulated EndMT and pro-fibrotic phenotype of ECs. These effects are related to the downregulation of Smad2/3. Conclusions: The study shows the pleiotropic effect of OA-NO2 on regulating EC-macrophage interactions during the immune response and suggests a role for OA-NO2 in the regulation of vascular endothelial immune and fibrotic responses arising during chronic inflammation. General significance: These findings propose the OA-NO2 may be useful as a novel therapeutic agent for treatment of cardiovascular disorders associated with dysregulation of the endothelial immune response. Twit Text FOAVip NITRO-OLEIC ACID INHIBITS VASCULAR ENDOTHELIAL INFLAMMATORY RESPONSES AND THE ENDOTHELIAL-MESENCHYMAL TRANSITION ????Biochim Biophys Acta http://www.kidney.de/pget.php?&tw=1&pmid=27431604 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27431604 #FOAvip English Wikipedia <ref>{{Cite pmid|27431604}}</ref> NITRO-OLEIC ACID INHIBITS VASCULAR ENDOTHELIAL INFLAMMATORY RESPONSES AND THE ENDOTHELIAL-MESENCHYMAL TRANSITION #MMPMID27431604 Ambrozova G; Fidlerova T; Martiskova H; Koudelka A; Rudolph TK; Woodcock SR; Freeman BA; Kubala L; Pekarova M Biochim Biophys Acta 2016[Nov]; 1860 (11 Pt A): 2428-37 PMID27431604show ga Background: Inflammatory-mediated pathological processes in the endothelium arise as a consequence of the dysregulation of vascular homeostasis. Of particular importance are mediators produced by stimulated monocytes/macrophages inducing activation of endothelial cells (ECs). This is manifested by excessive soluble pro-inflammatory mediator production and cell surface adhesion molecule expression. Nitro-fatty acids are endogenous products of metabolic and inflammatory reactions that display immuno-regulatory potential and may represent a novel therapeutic strategy to treat inflammatory diseases. The purpose of our study was to characterize the effects of nitro-oleic acid (OA-NO2) on inflammatory responses and the endothelial-mesenchymal transition (EndMT) in ECs that is a consequence of the altered healing phase of the immune response. Methods: The effect of OA-NO2 on inflammatory responses and EndMT was determined in murine macrophages and murine and human ECs using Western blotting, ELISA, immunostaining, and functional assays. Results: OA-NO2 limited the activation of macrophages and ECs by reducing pro-inflammatory cytokine production and adhesion molecule expression through its modulation of STAT, MAPK and NF-?B-regulated signaling. OA-NO2 also decreased transforming growth factor-?-stimulated EndMT and pro-fibrotic phenotype of ECs. These effects are related to the downregulation of Smad2/3. Conclusions: The study shows the pleiotropic effect of OA-NO2 on regulating EC-macrophage interactions during the immune response and suggests a role for OA-NO2 in the regulation of vascular endothelial immune and fibrotic responses arising during chronic inflammation. General significance: These findings propose the OA-NO2 may be useful as a novel therapeutic agent for treatment of cardiovascular disorders associated with dysregulation of the endothelial immune response. äNITRO-OLEIC ACID INHIBITS VASCULAR ENDOTHELIAL INFLAMMATORY RESPONSES (epmc).pdf DeepDyve Pubget Overpricing