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Fetal lung maturation in estrogen-deprived baboons.
J Clin Endocrinol Metab. 2003 Jan; 88(1):471-7.JC

Abstract

We have previously shown that estrogen plays a central integrative role in regulating key aspects of fetal-placental development and that inhibition of estrogen production during the second half of baboon pregnancy suppressed fetal adrenal function. Because maturation of the fetal lung is dependent on cortisol of fetal adrenal origin, the current study determined whether lung development and expression of surfactant proteins (SPs) A and B were altered at term in estrogen-deprived baboons. Fetal lungs were obtained on d 100, 165, and 175 of gestation (term = d 184) from untreated baboons and on d 165 from animals treated daily during the second half of pregnancy either with the aromatase inhibitor CGS 20267 alone or with CGS 20267 and estradiol benzoate. Umbilical venous estradiol levels were suppressed by more than 95% by CGS 20267 and elevated by CGS 20267 and estrogen. Although umbilical serum cortisol levels were also suppressed by 35% by CGS 20267, cortisol levels in the fetal lung of estrogen-suppressed baboons were similar to values in untreated animals. Immunocytochemistry demonstrated that CGS 20267 treatment did not alter fetal lung expression of the 11 beta-hydroxysteroid dehydrogenase enzyme-1 enzyme catalyzing reduction of cortisone to cortisol. However, immunocytochemical expression of the 11 beta-hydroxysteroid dehydrogenase enzyme-2 catalyzing oxidation of cortisol to cortisone appeared lower in lungs of estrogen-deprived fetuses and restored to normal by CGS 20267 and estrogen. SP-A levels in fetal lungs of untreated baboons were increased 16- to 20-fold between d 100 and d 165-175 of gestation in untreated baboons and baboons treated with CGS 20267 or CGS 20267 and estrogen. Similarly, SP-B levels in fetal lungs of untreated baboons were increased 10-fold between d 100 and d 165-175 of gestation in untreated baboons and baboons treated with CGS 20267 or CGS 20267 and estrogen. Moreover, in estrogen-suppressed baboons, as in untreated animals, the fetal lung continued to grow and exhibited normal alveolarization on histology. We conclude that development of the primate fetal lung can occur in utero in baboons in which fetal serum cortisol levels have been suppressed by the relative absence of estrogen perhaps because of the ability of the lung to coordinate local production of cortisol.

Authors+Show Affiliations

Department of Physiological Sciences, Eastern Virginia Medical School, Norfolk, Virginia 23501-1980, USA. pepegj@evms.eduNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

12519892

Citation

Pepe, Gerald J., et al. "Fetal Lung Maturation in Estrogen-deprived Baboons." The Journal of Clinical Endocrinology and Metabolism, vol. 88, no. 1, 2003, pp. 471-7.
Pepe GJ, Ballard PL, Albrecht ED. Fetal lung maturation in estrogen-deprived baboons. J Clin Endocrinol Metab. 2003;88(1):471-7.
Pepe, G. J., Ballard, P. L., & Albrecht, E. D. (2003). Fetal lung maturation in estrogen-deprived baboons. The Journal of Clinical Endocrinology and Metabolism, 88(1), 471-7.
Pepe GJ, Ballard PL, Albrecht ED. Fetal Lung Maturation in Estrogen-deprived Baboons. J Clin Endocrinol Metab. 2003;88(1):471-7. PubMed PMID: 12519892.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Fetal lung maturation in estrogen-deprived baboons. AU - Pepe,Gerald J, AU - Ballard,Philip L, AU - Albrecht,Eugene D, PY - 2003/1/10/pubmed PY - 2003/2/13/medline PY - 2003/1/10/entrez SP - 471 EP - 7 JF - The Journal of clinical endocrinology and metabolism JO - J Clin Endocrinol Metab VL - 88 IS - 1 N2 - We have previously shown that estrogen plays a central integrative role in regulating key aspects of fetal-placental development and that inhibition of estrogen production during the second half of baboon pregnancy suppressed fetal adrenal function. Because maturation of the fetal lung is dependent on cortisol of fetal adrenal origin, the current study determined whether lung development and expression of surfactant proteins (SPs) A and B were altered at term in estrogen-deprived baboons. Fetal lungs were obtained on d 100, 165, and 175 of gestation (term = d 184) from untreated baboons and on d 165 from animals treated daily during the second half of pregnancy either with the aromatase inhibitor CGS 20267 alone or with CGS 20267 and estradiol benzoate. Umbilical venous estradiol levels were suppressed by more than 95% by CGS 20267 and elevated by CGS 20267 and estrogen. Although umbilical serum cortisol levels were also suppressed by 35% by CGS 20267, cortisol levels in the fetal lung of estrogen-suppressed baboons were similar to values in untreated animals. Immunocytochemistry demonstrated that CGS 20267 treatment did not alter fetal lung expression of the 11 beta-hydroxysteroid dehydrogenase enzyme-1 enzyme catalyzing reduction of cortisone to cortisol. However, immunocytochemical expression of the 11 beta-hydroxysteroid dehydrogenase enzyme-2 catalyzing oxidation of cortisol to cortisone appeared lower in lungs of estrogen-deprived fetuses and restored to normal by CGS 20267 and estrogen. SP-A levels in fetal lungs of untreated baboons were increased 16- to 20-fold between d 100 and d 165-175 of gestation in untreated baboons and baboons treated with CGS 20267 or CGS 20267 and estrogen. Similarly, SP-B levels in fetal lungs of untreated baboons were increased 10-fold between d 100 and d 165-175 of gestation in untreated baboons and baboons treated with CGS 20267 or CGS 20267 and estrogen. Moreover, in estrogen-suppressed baboons, as in untreated animals, the fetal lung continued to grow and exhibited normal alveolarization on histology. We conclude that development of the primate fetal lung can occur in utero in baboons in which fetal serum cortisol levels have been suppressed by the relative absence of estrogen perhaps because of the ability of the lung to coordinate local production of cortisol. SN - 0021-972X UR - https://www.unboundmedicine.com/medline/citation/12519892/Fetal_lung_maturation_in_estrogen_deprived_baboons_ L2 - https://academic.oup.com/jcem/article-lookup/doi/10.1210/jc.2001-010228 DB - PRIME DP - Unbound Medicine ER -