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a Department of Physiology, University of Adelaide, Adelaide, South Australia 5005, Australia
b Department of Obstetrics and Gynecology, University of Wisconsin-Madison, Madison, Wisconsin 53715
Functional development of the adrenal cortex is critical for fetal maturation and postnatal survival. In the present study, we have determined the developmental profile of expression of the mRNA and protein of an essential cholesterol-transporting protein, steroidogenic acute regulatory protein (StAR), in the adrenal of the sheep fetus. We have also investigated the effect of placental restriction (PR) on the expression of StAR mRNA and protein in the growth-restricted fetus. Adrenal glands were collected from fetal sheep at 8291 days (n = 10), 125133 days (n = 10), and 140144 days (n = 9) and from PR fetuses at 141145 days gestation (n = 9) (term = 147 ± 3 days gestation). The adrenal StAR mRNA:18S rRNA increased (P < 0.05) between 125 days (7.44 ± 1.61) and 141144 days gestation (13.76 ± 1.88). There was also a 13-fold increase (P < 0.05) in the amount of adrenal StAR protein between 133 and 144 days gestation in these fetuses. However, the amount of StAR protein (6.9 ± 1.7 arbitrary densitometric units [AU]/µg adrenal protein) in the adrenal of the growth-restricted fetal sheep was significantly reduced, when compared with the expression of StAR protein (17.1 ± 1.9 AU/µg adrenal protein) in adrenals from the age-matched control group. In summary, there is a developmental increase in the expression of StAR mRNA and protein in the fetal sheep adrenal during the prepartum period when adrenal growth and steroidogenesis is dependent on ACTH stimulation. We have found that, while the level of expression of StAR protein is decreased in the adrenal gland of the growth-restricted fetus during late gestation, this does not impair adrenal steroidogenesis. Our data also suggest that the stimulation of adrenal growth and steroidogenesis in the growth-restricted fetus may not be ACTH dependent.
1 Supported in part by National Health and Medical Research Council of Australia 990275 (C.L.C.), Australian Research Council 9943135 (I.C.M.), National Institutes of Health grant HL56702 (I.M.B.), and United States Department of Agriculture 9601773 (I.M.B.). C.L.C. was supported by a J.B. Reid Fellowship from The University of Adelaide, South Australia.
2 Correspondence: Catherine L. Coulter, Department of Physiology, Medical School Building, The University of Adelaide, North Terrace, Adelaide, South Australia 5005, Australia. FAX: 61 8 8303 3356; catherine.coulter{at}adelaide.edu.au
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