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10.1155/2016/2174682 http://scihub22266oqcxt.onion/10.1155/2016/2174682 C4893598!4893598 !27313397     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27313397 &cmd=llinks): Failed to open stream: HTTP request failed! 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Inhibition of Macrophage Migration Inhibitory Factor Protects against Inflammation and Matrix Deposition in Kidney Tissues after Injury |pdf=|usr=}}{{27313397 }} gab.com Text Inhibition of Macrophage Migration Inhibitory Factor Protects against Inflammation and Matrix Deposition in Kidney Tissues after Injury JO: Mediators Inflamm http://www.kidney.de/pget.php?&tw=1&pmid=27313397 #FOAvip Background. Macrophage migration inhibitory factor (MIF) is an important immunoregulatory cytokine involved in inflammation, which may be one important reason resulting in matrix deposition in renal tissues after injury. However, the underlying mechanisms have not yet been elucidated. Methods and Results. We uncovered a crucial role of MIF in inflammation and collagen deposition in vivo and in vitro. In rats, ureteral obstruction induced tubular injury, matrix accumulation, and inflammatory cell infiltration. Additionally, enhanced MIF levels in the obstructed kidneys were closely related to the increasing numbers of CD68-positive macrophages. These obstruction-induced injuries can be relieved by recanalization, consequently resulting in downregulated expression of MIF and its receptor CD74. Similarly, ischemia reperfusion induced renal injury, and it was accompanied by elevated MIF levels and macrophages infiltration. In cultured tubular epithelial cells (TECs), aristolochic acid (AA) promoted matrix production and increased MIF expression, as well as the release of macrophage-related factors. Inhibition of MIF with an antagonist ISO-1 resulted in the abolishment of these genotypes in AA-treated TECs. Conclusion. MIF plays an important role in macrophage-related inflammation and matrix deposition in kidney tissues following injury. MIF as a specific inhibitor may have therapeutic potential for patients with inflammatory and fibrotic kidney diseases. Twit Text FOAVip Inhibition of Macrophage Migration Inhibitory Factor Protects against Inflammation and Matrix Deposition in Kidney Tissues after Injury ????Mediators Inflamm http://www.kidney.de/pget.php?&tw=1&pmid=27313397 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27313397 #FOAvip English Wikipedia <ref>{{Cite pmid|27313397 }}</ref> Inhibition of Macrophage Migration Inhibitory Factor Protects against Inflammation and Matrix Deposition in Kidney Tissues after Injury #MMPMID27313397 Lu H ; Bai Y ; Wu L ; Hong W ; Liang Y ; Chen B ; Bai Y Mediators Inflamm 2016[]; 2016 (ä): 2174682 PMID27313397 show ga Background. Macrophage migration inhibitory factor (MIF) is an important immunoregulatory cytokine involved in inflammation, which may be one important reason resulting in matrix deposition in renal tissues after injury. However, the underlying mechanisms have not yet been elucidated. Methods and Results. We uncovered a crucial role of MIF in inflammation and collagen deposition in vivo and in vitro. In rats, ureteral obstruction induced tubular injury, matrix accumulation, and inflammatory cell infiltration. Additionally, enhanced MIF levels in the obstructed kidneys were closely related to the increasing numbers of CD68-positive macrophages. These obstruction-induced injuries can be relieved by recanalization, consequently resulting in downregulated expression of MIF and its receptor CD74. Similarly, ischemia reperfusion induced renal injury, and it was accompanied by elevated MIF levels and macrophages infiltration. In cultured tubular epithelial cells (TECs), aristolochic acid (AA) promoted matrix production and increased MIF expression, as well as the release of macrophage-related factors. Inhibition of MIF with an antagonist ISO-1 resulted in the abolishment of these genotypes in AA-treated TECs. Conclusion. MIF plays an important role in macrophage-related inflammation and matrix deposition in kidney tissues following injury. MIF as a specific inhibitor may have therapeutic potential for patients with inflammatory and fibrotic kidney diseases. |Animals [MESH] |Antigens, CD/metabolism [MESH] |Antigens, Differentiation, Myelomonocytic/metabolism [MESH] |Aristolochic Acids/pharmacology [MESH] |Blotting, Western [MESH] |Cell Line [MESH] |Enzyme-Linked Immunosorbent Assay [MESH] |Epithelial Cells/drug effects/metabolism [MESH] |Epithelial-Mesenchymal Transition/drug effects [MESH] |Fluorescent Antibody Technique [MESH] |Immunohistochemistry [MESH] |Inflammation/*metabolism [MESH] |Intramolecular Oxidoreductases/antagonists & inhibitors/*metabolism [MESH] |Isoxazoles/pharmacology [MESH] |Kidney/immunology/*metabolism [MESH] |Macrophage Migration-Inhibitory Factors/antagonists & inhibitors/*metabolism [MESH] |Macrophages/drug effects/metabolism [MESH] |Male [MESH] |Rats [MESH] |Rats, Sprague-Dawley [MESH]Inhibition of Macrophage Migration Inhibitory Factor Protects against (epmc).pdf DeepDyve Pubget Overpricing