In this report, we demonstrate that NF-κB, a ubiquitous transcription factor, plays an essential role in silica-induced inflammatory mediator production in the mouse macrophage cell line RAW 264.7. Compared to the effect of lipopolysaccharide (LPS), silica mediated a stronger activation of NF-κB p50/p50 homodimer at early phase of poststimulation. Furthermore, activation of NF-κB by silica and LPS appears to be mediated by different signal transduction pathways. Both silica and LPS increased mRNA expression in these cells for cyclooxygenase II, inducible nitric oxide synthase, tumor necrosis factor-α and interleukin-1α. This expression was attenuated along with the inhibition of NF-κB activation.
|Original language||English (US)|
|Number of pages||8|
|Journal||Biochemical and Biophysical Research Communications|
|State||Published - Jan 1 1995|
All Science Journal Classification (ASJC) codes
- Molecular Biology
- Cell Biology