| First Author | Damoulis PD | Year | 1994 |
| Journal | Biochem Biophys Res Commun | Volume | 201 |
| Issue | 2 | Pages | 924-31 |
| PubMed ID | 8003032 | Mgi Jnum | J:19333 |
| Mgi Id | MGI:67504 | Doi | 10.1006/bbrc.1994.1790 |
| Citation | Damoulis PD, et al. (1994) Cytokines induce nitric oxide production in mouse osteoblasts. Biochem Biophys Res Commun 201(2):924-31 |
| abstractText | MC3T3-E1 mouse clonal osteogenic cells were incubated with interferon-gamma, interleukin-1 beta, tumor necrosis factor-alpha, and E. coli lipopolysaccharide. TNF alpha, IL-1 beta, and LPS caused a dose- and time-dependent increase of nitrite (NO2-), the stable metabolite of nitric oxide (NO), in conditioned media over 48 hours, while IFN gamma had a minimal effect. Different combinations of the same factors caused a synergistic enhancement of NO2- accumulation, except for IL-1 beta with LPS. The earliest detectable NO2- production was at 6-9 hours, with continued accumulation over 48 hours. NO2- production was inhibited dose-dependently by three arginine analogs known to be specific inhibitors of NO synthase, as well as by actinomycin D, cycloheximide, and dexamethasone; EGTA or indomethacin had a small inhibitory effect. It is concluded that osteoblast-like cells can be induced by proinflammatory cytokines and bacterial endotoxin to produce NO, which can play an important role in bone pathophysiology. |
