Multidirectional and simultaneous evaluation of gastroschisis-related intestinal damage in chick embryos
Muge Caglar1, Gungor Karaguzel1, Guzide Gokhan-Ocak2
1Akdeniz University School of Medicine, Department of Pediatric Surgery, Antalya, Turkey.
Insights
Gastroschisis-related intestinal damage (GRID) in chicks shows significant mucosal damage, reduced E-cadherin and synaptophysin, and increased apoptosis. These changes are linked to decreased NFκB and IκB expression, indicating a complex damaging process.
Area of Science:
- Developmental Biology
- Gastroenterology
- Pathology
Background:
- Gastroschisis is a congenital defect with significant intestinal damage.
- Understanding the underlying mechanisms of gastroschisis-related intestinal damage (GRID) is crucial for developing effective treatments.
Purpose of the Study:
- To investigate the morphological, cellular, molecular, and ultrastructural changes in the intestine of a chick model of gastroschisis.
Main Methods:
- A chick model was used, with gastroschisis created by an abdominal wall defect.
- Intestinal samples were analyzed using histopathology, immunohistochemistry, molecular biology, and electron microscopy.
Main Results:
- Histopathology revealed significantly higher intestinal damage in the gastroschisis group, primarily affecting mucosal structures.
- Immunohistochemistry showed decreased E-cadherin and synaptophysin, but unchanged laminin and type-4 collagen.
- Molecular analysis indicated reduced NFκB and IκB expression, with electron microscopy revealing apoptosis in all intestinal layers.
Conclusions:
- GRID impacts all intestinal layers, with the mucosa being most affected.
- Downregulation of E-cadherin and synaptophysin may contribute to the observed damage.
- Increased apoptosis, associated with decreased NFκB and IκB, is a key component of GRID.
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.
