Parturition Itself Is the Basis for Fetal Adrenal Involution

Ben-David, Shlomit; Zuckerman‐Levin, Nehama; Epelman, Mónica; Shen‐Orr, Zila; Levin, Moshe; Sujov, Polo; Hochberg, Zèev

doi:10.1210/jc.2005-2720

Cited by 31 publications

(21 citation statements)

References 34 publications

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“…Results of such studies also prove a dynamic increase in adrenal gland weight and their sudden involution in neonates [25][26][27][28][29].…”

Section: Adrenal Weight During Human Ontogenesismentioning

confidence: 78%

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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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“…Results of such studies also prove a dynamic increase in adrenal gland weight and their sudden involution in neonates [25][26][27][28][29].…”

Section: Adrenal Weight During Human Ontogenesismentioning

confidence: 78%

“…Moreover, not gestational age but parturition itself is the basis for fetal adrenal involution [29]. This implicates that placental factors are also involved in maintaining the fetal adrenal.…”

Section: Factors Regulating Human Fetal Adrenal Growth and Steroidogementioning

confidence: 99%

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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“…The triggering mechanism for this rapid, profound change in adrenal morphology, cellular architecture, and steroidogenesis is not known. It has been suggested that the involution of the fetal adrenal is more related to gestational age than to timing Articles after birth (19), but more recent studies indicate that parturition itself triggers fetal adrenal involution, which was interpreted as suggesting that the withdrawal of a placental factor stimulated the onset of fetal adrenal apoptosis (20). We hypothesize that the transition from intrauterine hypoxia to extrauterine normoxia is also a key event in triggering the remodeling of the fetal adrenal.…”

mentioning

confidence: 77%

“…Therefore, we and others have hypothesized that the involution of the fetal adrenal is not "programmed" but "triggered. " A current view is that the trigger is the loss of placental hormones and growth factors (20). Such a trigger could also be secondary to the profound environmental change that accompanies birth.…”

Section: Discussionmentioning

confidence: 99%

Potential role of increased oxygenation in altering perinatal adrenal steroidogenesis

et al. 2014

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Background: At birth, the large fetal adrenal involutes rapidly, and the patterns of steroidogenesis change dramatically; the event(s) triggering these changes remain largely unexplored. Fetal abdominal viscera receive hypoxic blood having a partial pressure of oxygen of only ~2 kPa (20-23 mm Hg); perinatal circulatory changes change this to adult values (~20 kPa). We hypothesized that transition from fetal hypoxia to postnatal normoxia participates in altering perinatal steroidogenesis. Methods: We grew midgestation human fetal adrenal cells and human NCI-H295A adrenocortical carcinoma cells in 2% O 2 , then transitioned them to 20% O 2 and quantitated steroidogenic mRNAs by quantitative PCR and microarrays. results: Transitioning fetal adrenal cells from hypoxia to normoxia increased mRNAs for 17α-hydroxylase/17,20 lyase (P450c17), 3β-hydroxysteroid dehydrogenase (3βHSD2), and steroidogenic acute regulatory protein (StAR). We repeated the protocol with NCI-H295A cells acclimated to hypoxia for 15 d, quantitating 31,255 transcripts by microarray. Using an arbitrary 1.5-fold difference, 1 d of normoxia increased 4 transcripts and decreased 56, whereas 2 d of normoxia increased 62 transcripts and decreased 105. P450c17, 3βHSD2, and StAR were ranked among the top eight increased transcripts. conclusion: These data suggest that the hypoxic/normoxic transition at birth contributes to perinatal changes in adrenal steroidogenesis.

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“…On the other hand, a centrally positioned fetal zone, responsible for androgen production during pregnancy, disappears during the postnatal period. In newborns, dramatic shrinkage of adrenal glands takes place due to involution of the fetal zone caused by apoptotic cell death (4,8). In rodents, as short gestational period species, adrenal glands synthesize glucocorticoids and aldosterone, but they are unable to produce androgens (9).…”

Section: Kratak Sadr`ajmentioning

confidence: 99%

Antenatal Treatment with Glucocorticoids and the Hypotalamic-Pituitary-Adrenal Axis

Manojlović‐Stojanoski¹,

Ristić²,

Singh³

et al. 2014

Journal of Medical Biochemistry

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SummaryFetal development is a critical period in the life cycle which is why the placenta provides a structural and physiological barrier that protects the fetus from the outer fluctuations and inner disturbances. A variety of influences from the environment, however, might induce fetal overexposure to glucocorticoids that target the fetal hypothalamic-pituitaryadrenal (HPA) axis and influence the fetal growth trajectory. Development of the HPA axis starts in the early stages of pregnancy, but the timing of HPA axis maturation and the glucocorticoid receptor (GR) expression in relation to birth is highly species-specific. The functional state of the fetal HPA axis plays a key role in the maturation of many organs necessary for intrauterine development and existence after birth. A functional HPA axis in near-term fetuses provides an adequate response to stress and also affects the timing of parturition. Due to their potent effect on the maturation of fetal tissues, synthetic glucocorticoids are used in human pregnancy at risk of preterm delivery. Dexamethasone and betamethasone, as the ones most commonly used, cross the placental enzymatic barrier (11b-hydroxysteroid dehydrogenase type 2 -11b-HSD2) and have 25-fold higher affinity to the GR than endogenous glucocorticoids, stimulating many aspects of fetal maturation. Despite the numerous positive effects, exposure to synthetic glucocorticoids during fetal development may result in intrauterine growth retardation and fetal programming of the HPA axis function which is associated with cardiovascular, metabolic and psychiatric disorders manifested later in life. Long-term consequences indicate the need for the implementation of new studies that will pro- Kratak sadr`ajFetalni razvoj predstavlja kriti~an period tokom `ivotnog ci klusa, zbog ~ega placenta obezbe|uje strukturnu i fiziolo{ku barijeru koja {titi fetus od spolja{njih kolebanja i unutra{njih poreme}aja. Brojni uticaji iz okru`enja mogu dovesti do izlaganja fetusa povi{enoj koncentraciji glukokor tikoida koji deluju na fetalnu hipotalamo-hipofiznoadrenalnu (HPA) oso vinu i uti~u na rast. Razvoj HPA osovine po~inje veoma rano tokom gestacije, ali vreme njenog sazrevanja i ekspresije glukokortikoidnog receptora (GR) u odnosu na ro|enje je specifi~no za svaku vrstu. Fetalna HPA osovina ima klju~nu ulogu u sazrevanju brojnih organa tokom intrauterinog raz voja neophodnih za pre`ivljavanje nakon ro|enja, obezbe |uje adekvatan odgovor fetusa na stres, a uti~e i na vreme poro|aja. Usled sna`nog uticaja na sazrevanje fetalnih tkiva, sintetski glukokortikoidi se upotrebljavaju tokom rizi~nih trudno}a kod kojih postoji opasnost od prevremenog poro|aja. Deksametazon i betametazon, kao naj~e{}e kori{}eni lekovi u antenatalnoj terapiji, prolaze enzimsku placentalnu barijeru (11b-hidroksisteroid dehidrogenaza tip 2 -11b-HSD2) i imaju 25 puta ve}i afinitet vezivanja za GR u odnosu na endogene gluko kortikoide, stimuli{u}i mnoge procese sazrevanja fetusa. Uprkos brojnim pozitivnim efektima, izlaganje sintetskim glukokorti...

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Parturition Itself Is the Basis for Fetal Adrenal Involution

Cited by 31 publications

References 34 publications

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

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

Potential role of increased oxygenation in altering perinatal adrenal steroidogenesis

Antenatal Treatment with Glucocorticoids and the Hypotalamic-Pituitary-Adrenal Axis

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