Enterocytic gene expression is altered in experimental gastroschisis.
Gastroschisis is a congenital anomaly in which exposure of the intestines to amniotic fluid throughout fetal life results in nutrient malabsorption. To begin to understand the molecular basis underlying epithelial changes in this condition, we investigated enterocytic gene expression during fetal development. Gastroschisis was surgically created at 24 days gestation (term = 31 days) in fetal rabbits; sham-operated and unoperated fetuses served as controls. Bowel was harvested at 28 and 31 days gestation. Cellular lactase expression was detected using immunohistochemistry, and apolipoprotein A-I and cellular retinol binding protein II (CRBPII) mRNA levels were quantitated using Northern blot analysis. Despite absence of gross histological changes in the mucosa, lactase protein expression and apolipoprotein A-I and CRBPII mRNA expression were decreased in intestine from gastroschisis compared to sham-operated animals. Expression of GAPDH (a housekeeping gene) increased over the same period, suggesting that the changes in enterocytic absorptive gene expression associated with gastroschisis were relatively specific. In conclusion, a decrease in expression of a variety of genes involved in nutrient absorption and trafficking within the enterocyte may contribute to the absorptive defects seen in this gastroschisis.
Srinathan
S K
SK
Department of Surgery, Washington University School of Medicine, St. Louis, Missouri 63110, USA.
Langer
J C
JC
Wang
J L
JL
Rubin
D C
DC
D000009:Abdominal Muscles / Q000002:abnormalities* / Q000378:metabolism / Q000473:pathology; D000818:Animals; D016632:Apolipoprotein A-I / Q000096:biosynthesis / Q000235:genetics; D001835:Body Weight; D003106:Colon / Q000033:anatomy & histology / Q000473:pathology; D004195:Disease Models, Animal; D005260:Female; D005313:Fetal Death; D015870:Gene Expression; D005987:Glyceraldehyde-3-Phosphate Dehydrogenases / Q000096:biosynthesis / Q000235:genetics; D006555:Hernia, Ventral / Q000151:congenital / Q000378:metabolism* / Q000473:pathology; D007413:Intestinal Mucosa / Q000378:metabolism*; D007422:Intestines / Q000002:abnormalities / Q000473:pathology; D043322:Lactase; D011247:Pregnancy; D012333:RNA, Messenger / Q000096:biosynthesis; D011817:Rabbits; D012177:Retinol-Binding Proteins / Q000096:biosynthesis / Q000235:genetics; D054840:Retinol-Binding Proteins, Cellular; D001616:beta-Galactosidase / Q000096:biosynthesis / Q000235:genetics
D016632:Apolipoprotein A-I; D012333:RNA, Messenger; D012177:Retinol-Binding Proteins; D054840:Retinol-Binding Proteins, Cellular; D005987:Glyceraldehyde-3-Phosphate Dehydrogenases; D043322:Lactase; D001616:beta-Galactosidase