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Am J Physiol Lung Cell Mol Physiol 274: L636-L646, 1998;
1040-0605/98 $5.00
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Vol. 274, Issue 4, L636-L646, April 1998

Inhibition of vascular and epithelial differentiation in murine nitrofen-induced diaphragmatic hernia

C. Coleman1, J. Zhao3, M. Gupta1, S. Buckley1, J. D. Tefft3, C. W. Wuenschell3, P. Minoo2,3, K. D. Anderson1, and D. Warburton1,3

1 Division of Pediatric Surgery and Developmental Biology Program, Childrens Hospital Los Angeles Research Institute, Los Angeles 90027; and 2 Divisions of Basic Research and Neonatology, Department of Pediatrics, Women and Children's Hospital, and 3 Center for Craniofacial and Molecular Biology, University of Southern California Schools of Medicine and Dentistry, Los Angeles, California 90033

Neonates with congenital diaphragmatic hernia (DH) die of pulmonary hypoplasia and persistent pulmonary hypertension. We used immunohistochemical localization of alpha -smooth muscle actin (alpha -SMA), platelet endothelial cell adhesion molecule (PECAM)-1, thyroid transcription factor (TTF)-1, surfactant protein (SP) A, SP-C, and competitive RT-PCR quantitation of TTF-1, SP-A, SP-C, and alpha -SMA mRNA expression to characterize the epithelial and vascular phenotype of lungs from ICR fetal mice with a nitrofen-induced DH. Nitrofen (25 mg) was gavage fed to pregnant mice on day 8 of gestation. Fetal mice were delivered on day 17. The diaphragm was examined for a defect, and the lungs were either fixed, sectioned, and immunostained or processed for mRNA isolation. In comparison with control lungs, DH lungs showed increased expression of alpha -SMA mRNA, fewer and more muscular arterioles (alpha -SMA), less well-developed capillary networks (PECAM-1), delayed epithelial development marked by a persistence of TTF-1 in the periphery, and decreased SP-A mRNA and SP-A expression. These data suggest that in the murine nitrofen-induced DH, as in human congenital DH, pulmonary insufficiency is due to an inhibition of peripheral pulmonary development including terminal airway and vascular morphogenesis.

pulmonary hypertension; pulmonary hypoplasia


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