Abstract
gastric epithelial cells as susceptible to both alcohol-induced cell damage (P=0.07) and apoptosis (P=0.06) as the gastric endothelial cells. Conversely, forced overexpression of survivin by transient transfection rendered gastric endothelial cells as resistant to both alcohol-induced cell damage (P=0.08) and apoptosis (P=0.06) as mock-transfected gastric epithelial cells. Moreover, overexpression of a threonine-34 to glutamate phosphorylation mimic mutant survivin construct rendered gastric endothelial cells significantly more resistant to alcohol-induced damage (P<0.02) and apoptosis (P<0.02) vs. mock-transfected gastric epithelial cells. CONCLUSIONS: 1) Disparate survivin expression levels can explain, in part, the discrepancy between gastric epithelial and endothelial cell susceptibility to alcoholinduced injury. 2) A negatively charged amino acid substitution at position 34, or the phosphorylation modification that naturally occurs on threonine-34 producing a negative charge at this position, increases the potency of survivin in mediating protection against alcohol-induced gastric mucosal cellular injury. (Supported by NIH R01AA14946)
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