Submucosal collagen in experimental gastroschisis.

Gastroschisis is a congenital anomaly in which the intestines are exposed to amniotic fluid throughout fetal life. Previous studies in animal models have demonstrated smooth muscle thickening and decreased contractility, epithelial dysfunction, and submucosal thickening. The present studies were done to further define the mechanism of submucosal changes by investigating collagen deposition and gene expression in a rabbit model. Gastroschisis was surgically created in fetal rabbits at 24 days gestation (term is 31 days). Sham-operated and unoperated fetuses served as controls. Fetuses were sacrificed and bowels were harvested at 26, 28, and 31 days gestation. Animal weight and gross and histologic appearance were assessed. Submucosal collagen content was measured using the van Geison stain. In situ hybridization of the expression of alpha (1) procollagen RNA was done to determine the distribution and source of submucosal collagen. At term, submucosal thickening was present in animals with gastroschisis, associated with a significantly increased collagen content. Collagen distribution was also more diffuse in the gastroschisis animals than in controls. In situ hybridization revealed procollagen expression in round cells located in the submucosa and not in smooth muscle. These cells did not resemble fibroblasts, and their identity is uncertain. Experimental gastroschisis is characterized by submucosal thickening which is associated with changes in collagen, including increased deposition and more diffuse distribution in the submucosa. The cells responsible for production of procollagen are round, nonfibroblast cells which are located in the submucosa and not in the smooth muscle layer. These findings may have some importance in understanding the mechanisms responsible for intestinal malfunction in infants with gastroschisis.