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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 Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27431604 &cmd=llinks): Failed to open stream: HTTP request failed! 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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 ; Verescakova H ; Koudelka A ; Rudolph TK ; Woodcock SR ; Freeman BA ; Kubala L ; Pekarova M Biochim Biophys Acta 2016[Nov]; 1860 (11 Pt A ): 2428-2437 PMID27431604 show 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. |*Epithelial-Mesenchymal Transition [MESH] |Animals [MESH] |Endothelial Cells/drug effects/metabolism [MESH] |Endothelium, Vascular/cytology/*drug effects/metabolism [MESH] |Humans [MESH] |Inflammation/metabolism [MESH] |MAP Kinase Signaling System [MESH] |Macrophages/drug effects/metabolism [MESH] |Mice [MESH] |NF-kappa B/metabolism [MESH] |Oleic Acids/*pharmacology [MESH] |STAT Transcription Factors/metabolism [MESH] |Smad Proteins/metabolism [MESH]Nitro-oleic acid inhibits vascular endothelial inflammatory responses (epmc).pdf DeepDyve Pubget Overpricing