Ectopic adrenocorticotropin (ACTH) and corticotropin‐releasing hormone (CRH) production in the adrenal gland: Basic and clinical aspects

Vrezas, Ilias; Willenberg, Holger S.; Mansmann, Georg; Hiroi, Naoki; Fritzen, Reimar; Bornstein, Stefan R.

doi:10.1002/jemt.10340

Cited by 31 publications

(24 citation statements)

References 51 publications

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“…This is similar to the situation in mammals where CRF and CRF-BP are present in the medulla, but not the cortex, of the adrenal gland (Nussdorfer 1996, Ehrhart-Bornstein et al 1998, Chatzaki et al 2002. The distribution of CRF in the chromaffin, but not the glucocorticoid compartment of vertebrates, is in agreement with their ontogenic roots: interrenal or adrenocortical cells are mesodermally derived, whereas the chromaffin cells originate from neural crest (Vrezas et al 2003). Apparently, the expression of neuropeptides or peptide hormones in the Figure 5 The effects of K C and 8-bromo-cAMP on the release of CRF and cortisol from superfused carp head kidneys.…”

Section: Discussionsupporting

confidence: 80%

Corticotropin-releasing factor (CRF) and CRF-binding protein expression in and release from the head kidney of common carp: evolutionary conservation of the adrenal CRF system

Huising

Metz

et al. 2007

Journal of Endocrinology

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Corticotropin-releasing factor (CRF) plays a central role in the regulation of the stress axis. In mammals, CRF as well as its receptors and its CRF-binding protein (CRF-BP) are expressed in a variety of organs and tissues outside the central nervous system. One of these extrahypothalamic sites is the adrenal gland, where the paracrine actions of adrenal CRF influence cortical steroidogenesis and adrenal blood flow. Although the central role of CRF signaling in the initiation and regulation of the stress response has now been established throughout vertebrates, information about the possible peripheral presence of CRF in earlier vertebrate lineages is scant. We established the expression of CRF, CRF-BP, and the CRF receptor 1 in a panel of peripheral organs of common carp (Cyprinus carpio). Out of all the peripheral organs tested, CRF and CRF-BP are most abundantly expressed in the carp head kidney, the fish equivalent of the mammalian adrenal gland. This expression localizes to chromaffin cells. Furthermore, detectable quantities of CRF are released from the intact head kidney following in vitro stimulation with 8-bromo-cAMP in a superfusion setup. The presence of CRF and CRF-BP within the chromaffin compartment of the head kidney suggests that a pathway homologous to the mammalian intraadrenal CRF system is present in the head kidney of fish. It follows that such a system to locally fine-tune the outcome of the centrally initiated stress response has been an integral part of the vertebrate endocrine system since the common ancestor of teleostean fishes and mammals.

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Section: Discussionsupporting

confidence: 80%

Corticotropin-releasing factor (CRF) and CRF-binding protein expression in and release from the head kidney of common carp: evolutionary conservation of the adrenal CRF system

Huising

Metz

et al. 2007

Journal of Endocrinology

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“…It was shown, that the CRH is also produced at several extrahypothalamic sites including the adrenal medulla (Udelsman et al, 1986;Bruhn et al, 1987;Venihaki et al, 1997;Vrezas et al, 2003). Several authors demonstrated that adrenals express the CRH type 1 and 2 receptors Vrezas et al, 2003).…”

Section: Discussionmentioning

confidence: 98%

Gene Expression of Phenylethanolamine N-Methyltransferase in Corticotropin-Releasing Hormone Knockout Mice During Stress Exposure

et al. 2006

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Data show that the CRH deficiency can markedly prevent immobilization-triggered induction of the PNMT mRNA and protein levels in the adrenal medulla and stellate ganglia. Reduced plasma epinephrine and corticosterone levels and adrenal medullary EGR-1 protein levels in CRH knockout versus WT mice during stress indicate that the HPA axis plays a crucial role in regulation of the PNMT gene expression in these organs. Cardiac atrial PNMT gene expression with stress is also dependent on intact HPA axis. However, in cardiac ventricles, especially after the single stress exposure, its expression is not impaired by CRH deficiency. Since cardiac EGR-1 protein levels in CRH KO mice are also not affected by the single stress exposure, we propose existence of different regulation of the PNMT gene expression, especially in the cardiac ventricles.Overall, our findings reveal that the PNMT gene expression is regulated through the HPA in both sympathoadrenal system and the heart and also via EGR-1 in the adrenal medulla, but apparently not in the heart. Regulation of the PNMT gene expression in various compartments of heart includes both corticosterone-dependent and independent mechanisms.

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“…ACTH is mainly produced in the corticotropic cells from the anterior pituitary, but is also produced in the brain, adrenal medulla, skin, and placenta (Vrezas et al 2003, Bicknell 2008, Evans et al 2012. As ACTH is the most potent stimulus of the adrenal cortex, most of the knowledge on its mechanism of action derives from studies on the adrenal cortex or ACTH receptor-expressing cells.…”

Section: Introductionmentioning

confidence: 99%

60 YEARS OF POMC: Adrenal and extra-adrenal functions of ACTH

Gallo‐Payet

2016

Journal of Molecular Endocrinology

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The pituitary adrenocorticotropic hormone (ACTH) plays a pivotal role in homeostasis and stress response and is thus the major component of the hypothalamo–pituitary–adrenal axis. After a brief summary of ACTH production from proopiomelanocortin (POMC) and on ACTH receptor properties, the first part of the review covers the role of ACTH in steroidogenesis and steroid secretion. We highlight the mechanisms explaining the differential acute vs chronic effects of ACTH on aldosterone and glucocorticoid secretion. The second part summarizes the effects of ACTH on adrenal growth, addressing its role as either a mitogenic or a differentiating factor. We then review the mechanisms involved in steroid secretion, from the classical Cyclic adenosine monophosphate second messenger system to various signaling cascades. We also consider how the interaction between the extracellular matrix and the cytoskeleton may trigger activation of signaling platforms potentially stimulating or repressing the steroidogenic potency of ACTH. Finally, we consider the extra-adrenal actions of ACTH, in particular its role in differentiation in a variety of cell types, in addition to its known lipolytic effects on adipocytes. In each section, we endeavor to correlate basic mechanisms of ACTH function with the pathological consequences of ACTH signaling deficiency and of overproduction of ACTH.

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Ectopic adrenocorticotropin (ACTH) and corticotropin‐releasing hormone (CRH) production in the adrenal gland: Basic and clinical aspects

Cited by 31 publications

References 51 publications

Corticotropin-releasing factor (CRF) and CRF-binding protein expression in and release from the head kidney of common carp: evolutionary conservation of the adrenal CRF system

Corticotropin-releasing factor (CRF) and CRF-binding protein expression in and release from the head kidney of common carp: evolutionary conservation of the adrenal CRF system

Gene Expression of Phenylethanolamine N-Methyltransferase in Corticotropin-Releasing Hormone Knockout Mice During Stress Exposure

60 YEARS OF POMC: Adrenal and extra-adrenal functions of ACTH

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