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B overexpression in cardiomyocytes prevents NF-B
translocation and provides cardioprotection in trauma
1 Department of Surgery and 2 Department of Pediatrics, The University of Texas Southwestern Medical Center, Dallas, Texas 75390-9160
This study examined the effects of either
I
B
overexpression (transgenic mice) or
N-acetyl-leucinyl-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. IB 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 factor-B (NF-B) nuclear
translocation, cardiomyocyte secretion of TNF-, and impaired cardiac
performance. IB overexpression or ALLN treatment of burn trauma
prevented NF-B activation in cardiac tissue, prevented cardiomyocyte
secretion of TNF-, and ablated burn-mediated cardiac contractile
dysfunction. These data suggest that NF-B activation and
inflammatory cytokine secretion play a significant role in postburn
myocardial abnormalities.
N-acetyl-leucinyl-leucinyl-norleucinal; collagenase digestion; cardiac contractile function; fura 2-AM
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