Functional zonation of the midgestation human fetal adrenal cortex: Fetal versus definitive zone use of progesterone for cortisol synthesis

Branchaud, Charlotte L.; Goodyer, Cynthia G.; Shore, Pamela; Lipowski, Lisa; Lefèbvre, Yves

doi:10.1016/0002-9378(85)90025-0

Cited by 11 publications

(4 citation statements)

References 17 publications

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“…In contrast, the activities of the enzymes catalyzing hydroxylations at steroid carbons 17, 21, and 11 (21,(54)(55)(56), as well as messenger RNAs (mRNAs) for the 17-and 21-hydroxylases (57)(58)(59), appear to be present earlier in gestation. These findings suggest that the baboon and monkey fetal adrenal have the capacity to synthesize cortisol from placental progesterone, as has been suggested in humans (60)(61)(62). However, based on in vivo studies in the baboon (63) and rhesus monkey (64), less than 5% of the cortisol meas- FETAL ADRENAL DEVELOPMENT 153 ured in fetal plasma during gestation is derived from circulating progesterone.…”

Section: Fetal Adrenal Developmentmentioning

confidence: 63%

Regulation of the Primate Fetal Adrenal Cortex*

1990

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Significant advances in our understanding of the regulation of fetal adrenal growth, differentiation, and steroidogenesis have been made in the past several years. In vitro studies employing molecular biological techniques have demonstrated that the placenta and several fetal tissues synthesize growth factors and/or oncogene-related products, which have the capacity to modulate growth and maturation of the fetal adrenal. Moreover, there is evidence that the fetal adrenal itself produces IGF-I and IGF-II and that the mRNAs for these growth factors are responsive to ACTH and perhaps other peptides originating in the fetal pituitary and/or the placenta. Most fascinating are the studies demonstrating that growth factors may also regulate the pattern of steroidogenesis elicited by the fetal adrenal. For example, TGF beta modulates binding, internalization, and degradation of LDL-cholesterol in adult adrenals while IGF-I increases fetal adrenal steroidogenesis by mechanisms that do not involve induction of P-450scc or enhanced metabolism of LDL. These studies, coupled with the observation that activation of protein kinase C by EGF or bFGF can block ACTH and/or other cAMP-induced increases in the activity of P-450(17 alpha), provide new insight into the subcellular mechanisms that underlie the regulation of fetal adrenal function. However, in vivo investigations must be aggressively pursued because the latter provide a major and perhaps exclusive means to elucidate the complex and multiple mechanisms that are apparently operative in utero in the regulation of fetal adrenal development. Moreover, in vivo studies remain the only valid means to delineate whether the factors that have been shown to modulate fetal adrenal function in vitro are indeed operable in vivo. Thus, in vivo investigations have shown that a multifactorial regulation of the fetal adrenal exists in utero in which PRL and perhaps other peptides as well as ACTH selectively stimulate fetal adrenal androgen production. Moreover, in vivo studies have demonstrated that a feedback mechanism operates in utero whereby estrogen produced in the placenta from androgen precursors of fetal adrenal origin feeds back to modulate the responsivity of the fetal adrenal to tropic peptides perhaps by regulating peptide binding to cell membrane receptors and/or other mechanisms. Evidence has also been provided from in vivo studies to support the concept that the placenta via metabolism of maternal cortisol and cortisone regulates fetal pituitary production of ACTH by modulating the extent to which maternal cortisol arrives at the fetus.(ABSTRACT TRUNCATED AT 400 WORDS)

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Section: Fetal Adrenal Developmentmentioning

confidence: 63%

Regulation of the Primate Fetal Adrenal Cortex*

1990

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“…Unlabeled steroids were purchased from Steraloids Inc. (Wilton, NH) and antisera to cortisol and dehydroepiandrosterone sulfate (DHAS) were from Endocrine Sciences (Tarzana, CA). Steroids were assayed directly, without prior extraction or chromatography of the media, as described previously (Branchaud et al, 1985). The levels of DHAS and cortisol in the medium containing 10% FBS were less than 1 ngiml, several thousand (DHASI-or several hundred (cortisol)-fold less than that produced by the cultured cells.…”

Section: Steroid Determinationsmentioning

confidence: 99%

“…Adrenals from one to four fetuses were used for each culture study. The fetal and definitive zones of the fetal adrenal were separated as described previously (Branchaud et al, 1978(Branchaud et al, , 1985. Fetal zone cells were obtained by collagenaseiDNAse dispersion as described previously (Abu-Hakima et al, 1987); they were suspended in Ham's F-10 culture medium containing 10% FBS (Hyclone Sterile Systems, Logan, UT) with antibiotics (200 IU penicillin G, Ayerst, Montreal, Que., Canada; 40 pgiml Gentamycin, Schering, Pointe-Claire, Que., Canada) and plated in 4.5 cm2 multiwell plastic dishes a t a concentration of 20,000-40,000 cellsiwell.…”

mentioning

confidence: 99%

Growth‐inhibitory effect of TGF‐B on human fetal adrenal cells in primary monolayer culture

Riopel

Branchaud

Goodyer

et al. 1989

Journal Cellular Physiology

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We examined the effects of transforming-growth factor-B (TGF-B) on growth ([3H]-thymidine uptake) and function (dehydroepiandrosterone sulfate [DHAS] and cortisol production) of human fetal zone adrenal cells. Results indicate that TGF-B significantly inhibits, in a dose-related manner, both basal and epidermal growth factor (EGF)-stimulated cell growth: IC50 = 0.1-0.25 ng/ml. EGF is ineffective in overcoming the inhibitory effect of TGF-B, suggesting a noncompetitive antagonism between the two factors. Also, the inhibitory effect of TGF-B is additive to that of adrenocorticotropic hormone (ACTH). On the other hand, TGF-B (1 ng/ml) does not significantly change basal or ACTH-stimulated DHAS or cortisol secretion. We conclude that, unlike its effect on other steroid-producing cells, TGF-B inhibits growth of fetal zone cells and does not appear to have a significant inhibitory effect on steroidogenesis.

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“…The studies demonstrated cortisol secretion by neocortex and DHEA/DHEAS by fetal zone as well as stimulating effects of ACTH on their secretion [93][94][95][96][97][98][99][100][101].…”

Section: Steroidogenesis In the Developing Human Adrenal Glandmentioning

confidence: 98%

100th anniversary of the discovery of the human adrenal fetal zone by Stella Starkel and Lesław Węgrzynowski: how far have we come?

Malendowicz

2011

Folia Histochem Cytobiol.

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Functional zonation of the midgestation human fetal adrenal cortex: Fetal versus definitive zone use of progesterone for cortisol synthesis

Cited by 11 publications

References 17 publications

Regulation of the Primate Fetal Adrenal Cortex*

Regulation of the Primate Fetal Adrenal Cortex*

Growth‐inhibitory effect of TGF‐B on human fetal adrenal cells in primary monolayer culture

100th anniversary of the discovery of the human adrenal fetal zone by Stella Starkel and Lesław Węgrzynowski: how far have we come?

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