| First Author | Hneino M | Year | 2012 |
| Journal | J Biol Chem | Volume | 287 |
| Issue | 46 | Pages | 38913-21 |
| PubMed ID | 22995913 | Mgi Jnum | J:192644 |
| Mgi Id | MGI:5465524 | Doi | 10.1074/jbc.M112.388389 |
| Citation | Hneino M, et al. (2012) The TG-interacting factor TGIF1 regulates stress-induced proinflammatory phenotype of endothelial cells. J Biol Chem 287(46):38913-21 |
| abstractText | The endothelium contributes to the control of the tissue inflammatory response following stress and in particular after exposure to ionizing radiation. We previously showed that the TG-interacting factor 1 (TGIF1) plays a role in radiation-induced normal tissue injury. In this study we hypothesized that this protein could play a role in inflammation. The role of TGIF1 in the stress-induced proinflammatory phenotype was investigated in human endothelial cells. In HUVECs ionizing radiation induces TGIF1 expression as well as a proinflammatory phenotype associated with up-regulation of IL-6, IL-8, CXCL1, MIP-2, and MCP-1. TGIF1 overexpression enhances the radiation-induced proinflammatory phenotype whereas TGIF1 silencing limits both the TNF-alpha- and radiation-induced overexpression of proinflammatory cytokines. Interestingly, in vivo, in radiation-induced intestinal inflammation in mice, TGIF1 genetic deficiency is associated with a reduced radiation-induced overexpression of proinflammatory molecules. In HUVECs, TNF-alpha- and radiation-induced NF-kappaB pathway activation is not influenced by TGIF1 expression, whereas TGIF1 knockdown inhibits both TNF-alpha- and radiation-induced p38 MAPK pathway activation. This study demonstrates that TGIF1 plays a role in TNF-alpha- and radiation-induced inflammation and suggests that it could be a target in limiting this event in the vascular compartment. |
