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10.1002/jcp.24870 http://scihub22266oqcxt.onion/10.1002/jcp.24870 C4519036!4519036 !25474999     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25474999 &cmd=llinks): Failed to open stream: HTTP request failed! 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Transcription factor MEF2C suppresses endothelial cell inflammation via regulation of NF-?B and KLF2 |pdf=|usr=}}{{25474999 }} gab.com Text Transcription factor MEF2C suppresses endothelial cell inflammation via regulation of NF- B and KLF2 JO: J Cell Physiol http://www.kidney.de/pget.php?&tw=1&pmid=25474999 #FOAvip Endothelial cells play a major role in the initiation and perpetuation of the inflammatory process in health and disease, including their pivotal role in leukocyte recruitment. The role of pro-inflammatory transcription factors in this process has been well-described, including NF-?B. However, much less is known regarding transcription factors that play an anti-inflammatory role in endothelial cells. Myocyte enhancer factor 2 C (MEF2C) is a transcription factor known to regulate angiogenesis in endothelial cells. Here, we report that MEF2C plays a critical function as an inhibitor of endothelial cell inflammation. Tumor necrosis factor (TNF)-? inhibited MEF2C expression in endothelial cells. Knockdown of MEF2C in endothelial cells resulted in the upregulation of pro-inflammatory molecules and stimulated leukocyte adhesion to endothelial cells. MEF2C knockdown also resulted in NF-?B activation in endothelial cells. Conversely, MEF2C overexpression by adenovirus significantly repressed TNF-? induction of pro-inflammatory molecules, activation of NF-?B, and leukocyte adhesion to endothelial cells. This inhibition of leukocyte adhesion by MEF2C was partially mediated by induction of KLF2. In mice, lipopolysaccharide (LPS)-induced leukocyte adhesion to the retinal vasculature was significantly increased by endothelial cell-specific ablation of MEF2C. Taken together, these results demonstrate that MEF2C is a novel negative regulator of inflammation in endothelial cells and may represent a therapeutic target for vascular inflammation. Twit Text FOAVip Transcription factor MEF2C suppresses endothelial cell inflammation via regulation of NF- B and KLF2 ????J Cell Physiol http://www.kidney.de/pget.php?&tw=1&pmid=25474999 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25474999 #FOAvip English Wikipedia <ref>{{Cite pmid|25474999 }}</ref> Transcription factor MEF2C suppresses endothelial cell inflammation via regulation of NF-?B and KLF2 #MMPMID25474999 Xu Z ; Yoshida T ; Wu L ; Maiti D ; Cebotaru L ; Duh EJ J Cell Physiol 2015[Jun]; 230 (6 ): 1310-20 PMID25474999 show ga Endothelial cells play a major role in the initiation and perpetuation of the inflammatory process in health and disease, including their pivotal role in leukocyte recruitment. The role of pro-inflammatory transcription factors in this process has been well-described, including NF-?B. However, much less is known regarding transcription factors that play an anti-inflammatory role in endothelial cells. Myocyte enhancer factor 2 C (MEF2C) is a transcription factor known to regulate angiogenesis in endothelial cells. Here, we report that MEF2C plays a critical function as an inhibitor of endothelial cell inflammation. Tumor necrosis factor (TNF)-? inhibited MEF2C expression in endothelial cells. Knockdown of MEF2C in endothelial cells resulted in the upregulation of pro-inflammatory molecules and stimulated leukocyte adhesion to endothelial cells. MEF2C knockdown also resulted in NF-?B activation in endothelial cells. Conversely, MEF2C overexpression by adenovirus significantly repressed TNF-? induction of pro-inflammatory molecules, activation of NF-?B, and leukocyte adhesion to endothelial cells. This inhibition of leukocyte adhesion by MEF2C was partially mediated by induction of KLF2. In mice, lipopolysaccharide (LPS)-induced leukocyte adhesion to the retinal vasculature was significantly increased by endothelial cell-specific ablation of MEF2C. Taken together, these results demonstrate that MEF2C is a novel negative regulator of inflammation in endothelial cells and may represent a therapeutic target for vascular inflammation. |Animals [MESH] |Cell Adhesion/physiology [MESH] |Cells, Cultured [MESH] |Endothelial Cells/*metabolism [MESH] |Endothelium, Vascular/metabolism [MESH] |Inflammation/immunology/metabolism [MESH] |Kruppel-Like Transcription Factors/*metabolism [MESH] |Leukocytes/metabolism [MESH] |Lipopolysaccharides/pharmacology [MESH] |MEF2 Transcription Factors/metabolism [MESH] |Mice [MESH] |NF-kappa B/*metabolism [MESH] |Signal Transduction/*physiology [MESH] |Tumor Necrosis Factor-alpha/metabolism [MESH]Transcription factor MEF2C suppresses endothelial cell inflammation vi(epmc).pdf DeepDyve Pubget Overpricing