Journal
CELLULAR IMMUNOLOGY
Volume 257, Issue 1-2, Pages 55-60Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.cellimm.2009.02.007
Keywords
HIN200; Endothelial cells; Inflammation; NF-kappa B; RNA interference
Categories
Funding
- Compagnia di San Paolo
- Ricerca Sanitaria Finalizzata
- Fondazione CRT
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The Interferon-inducible gene IFI16, a member of the HIN200 family, is activated by oxidative stress and cell density, in addition to Interferons, and it is implicated in the regulation of endothelial cell proliferation and vessel formation in vitro. We have previously shown that IFI16 is required for proinflammatory gene stimulation by IFN-gamma through the NF-kappa B complex. To examine whether IFI16 induction might be extended to other proinflammatory cytokines such as tumor necrosis factor (TNF)-alpha, we used the strategy of the RNA interference to knock down IFI16 expression, and analyze the capability of TNF-alpha to stimulate intercellular adhesion molecule-1 (ICAM-1 or CD54) expression in the absence of functional IFI16. Our studies demonstrate that IFI16 mediates ICAM-1 stimulation by TNF-alpha through the NF-kappa B pathway, thus reinforcing the role of the IFI16 molecule in the inflammation process. (C) 2009 Elsevier Inc. All rights reserved.
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