| First Author | Basílio J | Year | 2013 |
| Journal | Biochem Biophys Res Commun | Volume | 442 |
| Issue | 3-4 | Pages | 221-6 |
| PubMed ID | 24269235 | Mgi Jnum | J:211838 |
| Mgi Id | MGI:5576457 | Doi | 10.1016/j.bbrc.2013.11.030 |
| Citation | Basilio J, et al. (2013) TNFalpha-induced down-regulation of Sox18 in endothelial cells is dependent on NF-kappaB. Biochem Biophys Res Commun 442(3-4):221-6 |
| abstractText | The transcription factor Sox18 plays a role in angiogenesis, including lymphangiogenesis, where it is upregulated by growth factors and directs the expression of genes encoding, e.g., guidance molecules and a matrix metalloproteinase. Conversely, we found that in human umbilical vein endothelial cells (HUVEC) Sox18 is repressed by the pro-inflammatory mediator TNFalpha (as well as IL-1 and LPS). Since a common feature of these mediators is the activation of the NF-kappaB signaling pathway, we investigated whether Sox18 downregulation is dependent on this transcription factor. Transduction of HUVEC with an adenoviral vector directing the expression of the NF-kappaB inhibitor IkappaBalpha prevented the downregulation of Sox18. Transient transfections of Sox18 promoter reporter genes revealed that the downregulation takes place on the level of transcription, and that the p65/RelA subunit of NF-kappaB was operative. Furthermore, the responsible promoter region of Sox18 is located within -1.0kb from the transcriptional start site. The repression of Sox18 and its target genes may lead to altered formation of vessels in inflamed settings. |
