Cell-to-cell communication in bilateral macronodular adrenal hyperplasia causing hypercortisolism

It has been well established that, in the human adrenal gland, cortisol secretion is not only controlled by circulating corticotropin but is also influenced by a wide variety of bioactive signals, including conventional neurotransmitters and neuropeptides, released within the cortex by various cell...

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Main Authors: Herve eLefebvre, Celine eDuparc, Gaetan ePrevost, Jerome eBertherat, Estelle eLouiset
Format: Article
Language:English
Published: Frontiers Media S.A. 2015-04-01
Series:Frontiers in Endocrinology
Subjects:
Online Access:http://journal.frontiersin.org/Journal/10.3389/fendo.2015.00034/full
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author Herve eLefebvre
Herve eLefebvre
Herve eLefebvre
Celine eDuparc
Celine eDuparc
Gaetan ePrevost
Gaetan ePrevost
Gaetan ePrevost
Jerome eBertherat
Jerome eBertherat
Estelle eLouiset
Estelle eLouiset
author_facet Herve eLefebvre
Herve eLefebvre
Herve eLefebvre
Celine eDuparc
Celine eDuparc
Gaetan ePrevost
Gaetan ePrevost
Gaetan ePrevost
Jerome eBertherat
Jerome eBertherat
Estelle eLouiset
Estelle eLouiset
author_sort Herve eLefebvre
collection DOAJ
description It has been well established that, in the human adrenal gland, cortisol secretion is not only controlled by circulating corticotropin but is also influenced by a wide variety of bioactive signals, including conventional neurotransmitters and neuropeptides, released within the cortex by various cell types such as chromaffin cells, neurons, cells of the immune system, adipocytes and endothelial cells. These different types of cells are present in bilateral macronodular adrenal hyperplasia, a rare etiology of primary adrenal Cushing’s syndrome, where they appear intermingled with adrenocortical cells in the hyperplastic cortex. In addition, the genetic events which cause the disease favor abnormal adrenal differenciation that results in illicit expression of paracrine regulatory factors and their receptors in adrenocortical cells. All these defects constitute the molecular basis for aberrant autocrine/paracrine regulatory mechanisms which are likely to play a role in the pathophysiology of bilateral macronodular adrenal hyperplasia-associated hypercortisolism. The present review summarizes the current knowledge on this topic as well as the therapeutic perspectives offered by this new pathophysiological concept.
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spelling doaj.art-7dba23a3c959424ead2bd5775b4989a82022-12-22T02:58:27ZengFrontiers Media S.A.Frontiers in Endocrinology1664-23922015-04-01610.3389/fendo.2015.00034132518Cell-to-cell communication in bilateral macronodular adrenal hyperplasia causing hypercortisolismHerve eLefebvre0Herve eLefebvre1Herve eLefebvre2Celine eDuparc3Celine eDuparc4Gaetan ePrevost5Gaetan ePrevost6Gaetan ePrevost7Jerome eBertherat8Jerome eBertherat9Estelle eLouiset10Estelle eLouiset11Inserm U982/CHU et Université de RouenInstitute for Research and Innovation in Biomedicine, Rouen UniversityDepartment of Endocrinology, Diabetes and Metabolic Diseases, University Hospital of RouenInserm U982/CHU et Université de RouenInstitute for Research and Innovation in Biomedicine, Rouen UniversityInserm U982/CHU et Université de RouenInstitute for Research and Innovation in Biomedicine, Rouen UniversityDepartment of Endocrinology, Diabetes and Metabolic Diseases, University Hospital of RouenInstitut National de la Santé et de la Recherche Médicale, Unité 1016, Institut CochinDepartment of Endocrinology and Metabolic Diseases, Hôpital Cochin, Assistance Publique-Hôpitaux de ParisInserm U982/CHU et Université de RouenInstitute for Research and Innovation in Biomedicine, Rouen UniversityIt has been well established that, in the human adrenal gland, cortisol secretion is not only controlled by circulating corticotropin but is also influenced by a wide variety of bioactive signals, including conventional neurotransmitters and neuropeptides, released within the cortex by various cell types such as chromaffin cells, neurons, cells of the immune system, adipocytes and endothelial cells. These different types of cells are present in bilateral macronodular adrenal hyperplasia, a rare etiology of primary adrenal Cushing’s syndrome, where they appear intermingled with adrenocortical cells in the hyperplastic cortex. In addition, the genetic events which cause the disease favor abnormal adrenal differenciation that results in illicit expression of paracrine regulatory factors and their receptors in adrenocortical cells. All these defects constitute the molecular basis for aberrant autocrine/paracrine regulatory mechanisms which are likely to play a role in the pathophysiology of bilateral macronodular adrenal hyperplasia-associated hypercortisolism. The present review summarizes the current knowledge on this topic as well as the therapeutic perspectives offered by this new pathophysiological concept.http://journal.frontiersin.org/Journal/10.3389/fendo.2015.00034/fullHyperplasiaLeptinSerotoninACTHvasopressinendothelin
spellingShingle Herve eLefebvre
Herve eLefebvre
Herve eLefebvre
Celine eDuparc
Celine eDuparc
Gaetan ePrevost
Gaetan ePrevost
Gaetan ePrevost
Jerome eBertherat
Jerome eBertherat
Estelle eLouiset
Estelle eLouiset
Cell-to-cell communication in bilateral macronodular adrenal hyperplasia causing hypercortisolism
Frontiers in Endocrinology
Hyperplasia
Leptin
Serotonin
ACTH
vasopressin
endothelin
title Cell-to-cell communication in bilateral macronodular adrenal hyperplasia causing hypercortisolism
title_full Cell-to-cell communication in bilateral macronodular adrenal hyperplasia causing hypercortisolism
title_fullStr Cell-to-cell communication in bilateral macronodular adrenal hyperplasia causing hypercortisolism
title_full_unstemmed Cell-to-cell communication in bilateral macronodular adrenal hyperplasia causing hypercortisolism
title_short Cell-to-cell communication in bilateral macronodular adrenal hyperplasia causing hypercortisolism
title_sort cell to cell communication in bilateral macronodular adrenal hyperplasia causing hypercortisolism
topic Hyperplasia
Leptin
Serotonin
ACTH
vasopressin
endothelin
url http://journal.frontiersin.org/Journal/10.3389/fendo.2015.00034/full
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