Muge Caglar1, Gungor Karaguzel2, Guzide Gokhan-Ocak3, Duygu Yasar4, Sibel Berker-Karauzum4, Tekinalp Gelen3, Fatma Nur Celik5, Necdet Demir5, Mustafa Melikoglu1. 1. Akdeniz University School of Medicine, Department of Pediatric Surgery, Antalya, Turkey. 2. Akdeniz University School of Medicine, Department of Pediatric Surgery, Antalya, Turkey. Electronic address: gkaraguzel@akdeniz.edu.tr. 3. Akdeniz University School of Medicine, Department of Pathology, Antalya, Turkey. 4. Akdeniz University School of Medicine, Department of Medical Biology and Genetics, Antalya, Turkey. 5. Akdeniz University School of Medicine, Department of Histology and Embryology, Antalya, Turkey.
Abstract
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 NFκB and IκB 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 NFκB and IκB expression, may be an important component of this multifactorial damaging process.
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 NFκB and IκB 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 NFκB and IκB expression, may be an important component of this multifactorial damaging process.