title: Dual hormonal regulation of endocrine tissue mass and vasculature by adrenocorticotropin in the adrenal cortex.
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.
authors.affiliation: Institut National de la Santé et de la Recherche Médicale Equipe Mixte 105, DRDC-ANGIO, Commissariat à l'Energie Atomique, 17 rue des Martyrs, 38054 Grenoble Cedex 9, France.
authors.forename: Michael
authors.initials: M
authors.lastname: Thomas
authors.forename: Michelle
authors.initials: M
authors.lastname: Keramidas
authors.forename: Emmanuelle
authors.initials: E
authors.lastname: Monchaux
authors.forename: Jean-Jacques
authors.initials: JJ
authors.lastname: Feige
mesh_terms: D000302:Adrenal Cortex / Q000098:blood supply* / Q000473:pathology / Q000502:physiology*; D000324:Adrenocorticotropic Hormone / Q000097:blood* / Q000378:metabolism; D000818:Animals; D017209:Apoptosis / Q000187:drug effects / Q000502:physiology; D001284:Atrophy; D002455:Cell Division / Q000187:drug effects / Q000502:physiology; D003907:Dexamethasone / Q000494:pharmacology; D015536:Down-Regulation; D004730:Endothelium, Vascular / Q000166:cytology / Q000187:drug effects / Q000502:physiology; D005938:Glucocorticoids / Q000494:pharmacology; D008297:Male; D051379:Mice; D008815:Mice, Inbred Strains; D018919:Neovascularization, Physiologic / Q000187:drug effects / Q000502:physiology*; D012333:RNA, Messenger / Q000032:analysis; D042461:Vascular Endothelial Growth Factor A / Q000235:genetics / Q000378:metabolism
chemical_list: D005938:Glucocorticoids; D012333:RNA, Messenger; D042461:Vascular Endothelial Growth Factor A; D003907:Dexamethasone; D000324:Adrenocorticotropic Hormone