Dual hormonal regulation of endocrine tissue mass and vasculature by adrenocorticotropin in the adrenal cortex.
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TLDR
The data support the concept that ACTH controls adrenal cortex trophicity through a dual mechanism involving its antiapoptotic effect on endocrine cells and its indirect vascular endothelial growth factor-mediated action on endothelial cells.Abstract:
The mass of healthy adult tissues is stable and their vasculature is quiescent, but this equilibrium is disrupted under certain physiological or pathological situations. There is an emerging concept indicating that these trophic changes may be initiated by modifications of the vasculature. In the current study, we documented over a period of 14 d the serial alterations occurring in both endocrine and endothelial compartments during adrenal atrophy induced by ACTH suppression in mice. After dexamethasone perfusion, a rapid fall of plasmatic ACTH and corticosterone concentrations was observed within the first 24 h. During the first 4 d of treatment, adrenal weight and adrenal cortex cellularity decreased rapidly. This was correlated with an inhibition of cell proliferation and a massive induction of endocrine cell apoptosis. Between d 4 and d 14, a slower but sustained decay of adrenal cortex size and cellularity was observed. This second phase was associated with progressive loss of vascular endothelial growth factor protein expression in the endocrine cells and regression of the vascular network. These data support the concept that ACTH controls adrenal cortex trophicity through a dual mechanism involving its antiapoptotic effect on endocrine cells and its indirect vascular endothelial growth factor-mediated action on endothelial cells.read more
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Development and function of the human fetal adrenal cortex: a key component in the feto-placental unit.
Hitoshi Ishimoto,Robert B. Jaffe +1 more
TL;DR: Mounting evidence indicates that actions of hormones operating in the human feto-placental unit are likely mediated by mechanisms including target tissue responsiveness, local metabolism, and bioavailability, rather than changes only in circulating levels.
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Hypothalamic-pituitary-adrenocortical axis regulation.
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Intraadrenal Corticotropin in Bilateral Macronodular Adrenal Hyperplasia
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TL;DR: Cortisol secretion by the adrenals in patients with macronodular hyperplasia and Cushing's syndrome appears to be regulated by corticotropin, which is produced by a subpopulation of steroidogenic cells in the hyperplastic adrenals.
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Hypothalamic-pituitary-adrenocortical axis: neuropsychiatric aspects.
TL;DR: Greater attention to patient heterogeneity and more consistent approaches to assessing treatment effects on HPA function may solidify the value of HPA measures in predicting treatment response or developing novel strategies to manage psychiatric disease.
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Cushing's Syndrome and Fetal Features Resurgence in Adrenal Cortex–Specific Prkar1a Knockout Mice
Isabelle Sahut-Barnola,Cyrille de Joussineau,Pierre Val,Sarah Lambert-Langlais,Christelle Damon,Anne-Marie Lefrançois-Martinez,Jean-Christophe Pointud,G. Marceau,V. Sapin,Frédérique Tissier,Bruno Ragazzon,Jérôme Bertherat,Lawrence S. Kirschner,Constantine A. Stratakis,Antoine Martinez +14 more
TL;DR: The data provide the first in vivo evidence that loss of R1α is sufficient to induce autonomous adrenal hyper-activity and bilateral hyperplasia, both observed in human PPNAD, and demonstrates that deregulated PKA activity favors the emergence of a new cell population potentially arising from the fetal adrenal, giving new insight into the mechanisms leading to PPN AD.
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