I B overexpression in cardiomyocytes prevents NF- B translocation and provides cardioprotection in trauma

Carlson, Deborah L., D. Jean White, David L. Maass, Robin C. Nguyen, Brett Giroir, and Jureta W. Horton. I B overexpression in cardiomyocytes prevents NFB translocation and provides cardioprotection in trauma. Am J Physiol Heart Circ Physiol 284: H804–H814, 2003; 10.1152/ ajpheart.00394.2001.—This study examined the effects of either I B overexpression (transgenic mice) or N-acetylleucinyl-leucinyl-norleucinal (ALLN) administration (proteosome inhibitor in wild-type mice) on cardiomyocyte secretion of tumor necrosis factor(TNF) and on cardiac performance after burn trauma. Transgenic mice were divided into four experimental groups. I B overexpressing mice were given a third-degree scald burn over 40% of the total body surface area or wild-type littermates were given either a scald or sham burn to provide appropriate controls. Pharmacological studies included ALLN (20 mg/kg) administration in either burned wild-type mice or wild-type shams. Burn trauma in wild-type mice promoted nuclear factorB (NFB) nuclear translocation, cardiomyocyte secretion of TNF, and impaired cardiac performance. I B overexpression or ALLN treatment of burn trauma prevented NFB activation in cardiac tissue, prevented cardiomyocyte secretion of TNF, and ablated burn-mediated cardiac contractile dysfunction. These data suggest that NFB activation and inflammatory cytokine secretion play a significant role in postburn myocardial abnormalities.