Hoath S B, Pickens W L, Sells S F, Boissy R E
Department of Pediatrics & Dermatology, Children's Hospital Medical Center, Cincinnati, Ohio 45267.
J Dev Physiol. 1990 Jan;13(1):41-50.
Intrauterine growth retardation (IUGR) due to vascular insufficiency in humans results in newborn infants with marked loss of subcutaneous fat and a poorly characterized "dysmature" appearance of the epidermis. In this study, we examined selected indices of epidermal development in 20 and 21 day old growth retarded fetal rats. IUGR was produced by unilateral ligation of the uterine artery and vein on gestational day 17. Littermate rats from the opposite uterine horn were utilized as pair matched experimental controls. A total of 49 consecutive fetal pairs were examined. Mean body weight (+/- SEM) for controls was 4.2 +/- 0.1 g versus 2.6 +/- 0.2 g for the treatment group on gestational day 20 (n = 74, P less than 0.01) and 6.0 +/- 0.1 versus 4.0 +/- 0.2 g, respectively, on the day 21 (n = 24, P less than 0.01). Examination by light and electron microscopy showed marked diminution in overall epidermal thickness in the growth retarded animals, particularly of the stratum granulosum and stratum corneum. Epidermal DNA content was decreased in IUGR pups on day 20 (0.99 +/- 0.05 versus 1.26 +/- 0.07 micrograms DNA/mg wet weight, P less than 0.05). Soluble epidermal proteins showed a similar reduction in IUGR animals (30.2 + 0.8 versus 34.7 +/- 1.6 micrograms protein/mg wet weight, P less than 0.05). IUGR also decreased the total amount of epidermal protein extractable in 8 M urea. Differentiation-specific epidermal proteins (keratins, filaggrin) were markedly reduced in the growth retarded animals following normalization to epidermal surface area and analysis by polyacrylamide gel electrophoresis. Overall, these changes in the growth retarded fetal rat lead to formation of a thin, hypoplastic, and poorly keratinized epidermal covering.