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Transcription Factor MEF2C Suppresses Endothelial Cell Inflammation via Regulation of NF‐κB and KLF2

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‐κB. 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)‐α 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‐κB activation in endothelial cells. Conversely, MEF2C overexpression by adenovirus significantly repressed TNF‐α induction of pro‐inflammatory molecules, activation of NF‐κB, 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. J. Cell. Physiol. 230: 1310–1320, 2015. © 2014 Wiley Periodicals, Inc., A Wiley Company