JOURNAL OF PEDIATRIC SURGERY, cilt.49, sa.11, ss.1577-1584, 2014 (SCI-Expanded)
Purpose: In a chick model of gastroschisis, we aimed to investigate the morphological/cellular, molecular, and ultrastructural changes taking place in gastroschisis-related intestinal damage (GRID). Methods: 13-Day fertilized eggs were divided into two groups. Control group: chorio-amnio-allontoic membranes opened and abdominal wall exposed. Gastroschisis group: an anterior abdominal wall defect created after opening membranes. Embryos from both groups were surgically removed on post-fertilization day 19. Intestinal samples were obtained for histopathology, immunohistochemistry, molecular biology, and electron microscopy. Results: The histopathological grade of intestinal damage which primarily involved mucosal structures was significantly higher in the gastroschisis group when compared to the control group (p < 0.001). Immunohistochemically, E-cadherin and synaptophysin immunoreactivity in the gastroschisis group was significantly lower than control group (p < 0.05 and p < 0.01, respectively), whereas there was no significant difference in laminin and type-4 collagen immunoreactivity between the groups (p > 0.05). Molecular analyses indicated a significant decrease in NF kappa B and I kappa B expression in the gastroschisis group (p < 0.05 and p = 0.001, respectively). Electron microscopy showed that the gastroschisis group had considerable ultrastructural damage, manifested by apoptosis in all layers. Conclusions: GRID affected all layers but was more prominent in mucosa. The damage may depend on E-cadherin and synaptophysin downregulation. Increased apoptotic activity, associated with decreased NF kappa B and I kappa B expression, may be an important component of this multifactorial damaging process. (C) 2014 Elsevier Inc. All rights reserved.