Literature DB >> 15695100

Estrogen/hypothalamus-pituitary-adrenal axis interactions in the fetus: The interplay between placenta and fetal brain.

Charles E Wood1.   

Abstract

OBJECTIVE: The hormonal interactions between the placenta and the fetal hypothalamus-pituitary-adrenal (HPA) axis are reviewed.
METHODS: This review addresses data obtained from the chronically catheterized fetal sheep, drawing relevant comparisons to human fetuses.
RESULTS: In the sheep, and perhaps in primate species, parturition is initiated by an increase in the activity of the HPA axis. The endogenous mechanisms underlying the increase in activity of the fetal HPA axis are incompletely understood but might involve an interplay between placenta and fetal hypothalamus and pituitary. Various hypotheses have been proposed, involving placental secretion of prostaglandins and various components of the fetal HPA axis. In the sheep, the influence of estradiol appears to be potent, and various experiments have suggested the possibility that, in late gestation, there exists a positive feedback relationship between placental estrogen secretion and pituitary adrenocorticotropin (ACTH) secretion. Estradiol circulates in concentrations known to stimulate fetal ACTH secretion. Additionally, estradiol circulates in the form of estradiol-3-sulfate, a molecular form that is taken up by the fetal brain and deconjugated by steroid sulfatase, which is expressed in the fetal brain. Recent evidence suggests that the interaction between estradiol and ACTH might involve production of paracrine or autocrine substances in the fetal brain. One candidate mediator is prostaglandin E2 (PGE2), highlighted by the action of estradiol on the expression of prostaglandin endoperoxide synthase-2 (PGHS-2 or COX-2) in brain regions known to be important for controlling HPA activity.
CONCLUSION: Estradiol, secreted by the placenta in increasing amounts in late gestation, is a potent stimulator of fetal ACTH secretion. The interactions between estradiol and the fetal HPA axis might function as a positive feedback loop that increases the concentrations of both hormones before birth.

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Year:  2005        PMID: 15695100     DOI: 10.1016/j.jsgi.2004.10.011

Source DB:  PubMed          Journal:  J Soc Gynecol Investig        ISSN: 1071-5576


  16 in total

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Journal:  Front Neuroendocrinol       Date:  2008-03-05       Impact factor: 8.606

2.  Ontogeny of androgen receptor expression in the ovine fetal central nervous system and pituitary.

Authors:  Charles E Wood; Maureen Keller-Wood
Journal:  Neurosci Lett       Date:  2008-05-08       Impact factor: 3.046

Review 3.  Epigenetic impacts of endocrine disruptors in the brain.

Authors:  Deena M Walker; Andrea C Gore
Journal:  Front Neuroendocrinol       Date:  2016-09-20       Impact factor: 8.606

4.  Influence of estradiol and fetal stress on luteinizing hormone, follicle-stimulating hormone, and prolactin in late-gestation fetal sheep.

Authors:  Charles E Wood; Maureen Keller-Wood
Journal:  Neonatology       Date:  2011-03-24       Impact factor: 4.035

5.  Triclosan is a potent inhibitor of estradiol and estrone sulfonation in sheep placenta.

Authors:  Margaret O James; Wenjun Li; David P Summerlot; Laura Rowland-Faux; Charles E Wood
Journal:  Environ Int       Date:  2009-03-18       Impact factor: 9.621

6.  Inhibition of brain prostaglandin endoperoxide synthase-2 prevents the preparturient increase in fetal adrenocorticotropin secretion in the sheep fetus.

Authors:  Jason Gersting; Christine E Schaub; Maureen Keller-Wood; Charles E Wood
Journal:  Endocrinology       Date:  2008-05-01       Impact factor: 4.736

7.  17beta-estradiol protects against hypoxic/ischemic white matter damage in the neonatal rat brain.

Authors:  Bettina Gerstner; Joan Lee; Tara M DeSilva; Frances E Jensen; Joseph J Volpe; Paul A Rosenberg
Journal:  J Neurosci Res       Date:  2009-07       Impact factor: 4.164

8.  Administration of low dose triclosan to pregnant ewes results in placental uptake and reduced estradiol sulfotransferase activity in fetal liver and placenta.

Authors:  Erin N Jackson; Laura Rowland-Faux; Margaret O James; Charles E Wood
Journal:  Toxicol Lett       Date:  2018-05-26       Impact factor: 4.372

9.  Blockade of estrogen receptors decreases CNS and pituitary prostaglandin synthase expression in fetal sheep.

Authors:  Christine E Schaub; Maureen Keller-Wood; Charles E Wood
Journal:  Neuroendocrinology       Date:  2007-10-09       Impact factor: 4.914

10.  Blockade of estrogen action upregulates estrogen receptor-alpha mRNA in the fetal brain.

Authors:  Christine E Schaub; Charles E Wood
Journal:  Neonatology       Date:  2009-03-12       Impact factor: 4.035

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