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Enterocytic gene expression is altered in experimental gastroschisis
S K Srinathan1, J C Langer, J L Wang
1Department of Surgery, Washington University School of Medicine, St. Louis, Missouri 63110, USA.
The Journal of Surgical Research
|February 15, 1997
Summary
Gastroschisis, a congenital defect, impairs nutrient absorption due to intestinal exposure to amniotic fluid. This study reveals decreased expression of key absorptive genes in fetal rabbit intestines, contributing to malabsorption.
Area of Science:
- Developmental biology
- Gastroenterology
- Molecular biology
Background:
- Gastroschisis is a congenital anomaly leading to intestinal malabsorption.
- The molecular mechanisms underlying these absorptive defects are not fully understood.
Purpose of the Study:
- To investigate enterocytic gene expression during fetal development in gastroschisis.
- To identify molecular changes contributing to nutrient malabsorption in gastroschisis.
Main Methods:
- Surgically created gastroschisis in fetal rabbits at 24 days gestation.
- Harvested bowel at 28 and 31 days gestation for analysis.
- Quantified lactase protein, apolipoprotein A-I, and CRBPII mRNA levels using immunohistochemistry and Northern blot analysis.
Main Results:
- Decreased lactase protein expression in gastroschisis intestines compared to controls.
- Reduced apolipoprotein A-I and CRBPII mRNA levels in gastroschisis intestines.
- Specific downregulation of absorptive genes, not general changes, as indicated by GAPDH expression.
Conclusions:
- Reduced expression of nutrient absorption and trafficking genes in enterocytes may cause absorptive defects in gastroschisis.
- These molecular changes occur despite the absence of gross histological alterations.
- This study provides insight into the molecular basis of gastroschisis-associated malabsorption.