Upregulation of 14-3-3 isoforms in acute rat myocardial injuries induced by burn and lipopolysaccharide.

1. Burn-induced myocardial injuries can be acute due to loss of body fluid and blood redistribution, and subacute due to pathogenic toxins of infecting bacteria. The goal of this study was to examine expression of 14-3-3 in the injured myocardium. 2. Myocardial injury models were created in vivo by subjecting rats to severe burn and administration of lipopolysaccharide. RT-PCR and Western blotting were employed to assess the expression of 14-3-3 proteins and messenger ribonucleic acid (mRNA) for 14-3-3eta and gamma in the myocardium, respectively. 3. In the two models, we found that 14-3-3 proteins were induced in a time-dependent fashion. Such a change is at least in part attributed to increases in mRNAs for 14-3-3gamma and eta. In contrast to 14-3-3xi, whose mRNA was not detectable in the heart, mRNA for 14-3-3gamma was found significantly elevated between 24-48 h after burn. 14-3-3eta mRNA exhibited a marked increase at 3 h continuing to 12 h and then decreased nearly to a normal level after 48 h. In lipopolysaccharide-treated intact rats, 14-3-3gamma mRNA in myocardium showed a significant increase, reaching a peak at 4 h, followed by a decrease at 6 h. In contrast, 14-3-3eta mRNA had a slight increase without significance. 4. Our results suggest that 14-3-3 may play a role in both acute and subacute (postburn infectious) phases of severe burn.