Past, Present and Future of Human Chromaffin Cells: Role in Physiology and Therapeutics

Pérez-Álvarez, Alberto; Hernández‐Vivanco, Alicia; Albillos, Almudena

doi:10.1007/s10571-010-9582-0

Cited by 15 publications

(10 citation statements)

References 109 publications

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“…Catecholamine secretion usually takes place in situations of fear, anxiety or organic stress. However, the release of hormones from adrenomedullary chromaffin cells can also be triggered by a number of chemicals that reach the adrenal medulla via the bloodstream [129]. For this reason, in recent years several in vitro studies have been performed in order to verify the endocrine disrupting activity of NPs (especially metal-based NPs), on chromaffin cells (see Table 5).…”

Section: Impact Of Endocrine Disrupting Nps On the Neuroendocrine mentioning

confidence: 99%

The Effects of Nanomaterials as Endocrine Disruptors

Iavicoli

Fontana

Leso

et al. 2013

IJMS

200

120

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In recent years, nanoparticles have been increasingly used in several industrial, consumer and medical applications because of their unique physico-chemical properties. However, in vitro and in vivo studies have demonstrated that these properties are also closely associated with detrimental health effects. There is a serious lack of information on the potential nanoparticle hazard to human health, particularly on their possible toxic effects on the endocrine system. This topic is of primary importance since the disruption of endocrine functions is associated with severe adverse effects on human health. Consequently, in order to gather information on the hazardous effects of nanoparticles on endocrine organs, we reviewed the data available in the literature regarding the endocrine effects of in vitro and in vivo exposure to different types of nanoparticles. Our aim was to understand the potential endocrine disrupting risks posed by nanoparticles, to assess their underlying mechanisms of action and identify areas in which further investigation is needed in order to obtain a deeper understanding of the role of nanoparticles as endocrine disruptors. Current data support the notion that different types of nanoparticles are capable of altering the normal and physiological activity of the endocrine system. However, a critical evaluation of these findings suggests the need to interpret these results with caution since information on potential endocrine interactions and the toxicity of nanoparticles is quite limited.

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Section: Impact Of Endocrine Disrupting Nps On the Neuroendocrine mentioning

confidence: 99%

The Effects of Nanomaterials as Endocrine Disruptors

Iavicoli

Fontana

Leso

et al. 2013

IJMS

200

120

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“…Here the chromaffi n cells secrete around 80 % adrenaline (epinephrine) and 20 % noradrenaline (norepinephrine), whereas this proportion is reversed in the sympathetic nerves, which contain predominantly noradrenaline [ 41 ]. The adrenergic and noradrenergic secretion in different groups of chromaffi n cells relies on the different α 2 AR subtypes' expression [ 59 ]. The adrenal gland can be compared to a specialized sympathetic ganglion, receiving inputs from the sympathetic nervous system via preganglionic fi bers.…”

Section: Adrenergic Signaling In Cardiovascular Aging and Heart Failurementioning

confidence: 99%

Sympathetic Nervous System Signaling in Heart Failure and Cardiac Aging

Santulli

2015

Pathophysiology and Pharmacotherapy of Cardiovascular Disease

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Heart failure represents the leading cause of death, especially among the elderly. Despite the development of numerous therapeutic strategies, heart failure prevalence is still increasing. Ergo, exploring the molecular mechanisms underlying aging-related heart failure seems to be of particular relevance. Intriguingly, the fi elds of cardiovascular disease and aging, which have remained largely separate hitherto, seem to have a common point in the sympathetic nervous system. Indeed, mounting evidence indicates that adrenergic receptors are functionally involved in numerous processes underlying both aging and cardiovascular disease. This chapter will review the pathophysiological role of the sympathetic nervous system in heart failure and cardiac aging.

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“…Sympathetic excitation activates chromaffin cells to release catecholamines and peptide transmitters into the circulation, affecting a broad spectrum of functions including blood pressure, cardiac output and blood glucose as well as afferent sensory activity (Vollmer et al, 1997; Habib et al, 2001). Improper transmitter release from the adrenal can lead to complex disease states including hypertension, diabetes, and cardiomyopathy (Perez-Alvarez et al, 2010). Catecholamines and peptide transmitters are co-packed in the same secretory granules (Winkler and Westhead, 1980; Crivellato et al, 2008); however, they are differentially secreted in an activity-dependent manner.…”

Section: Introductionmentioning

confidence: 99%

Activity-Dependent Fusion Pore Expansion Regulated by a Calcineurin-Dependent Dynamin-Syndapin Pathway in Mouse Adrenal Chromaffin Cells

Samasilp¹,

Chan²,

Smith³

2012

Journal of Neuroscience

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Neuroendocrine chromaffin cells selectively secrete a variety of transmitter molecules into the circulation as a function of sympathetic activation. Activity-dependent release of transmitter species is controlled through regulation of the secretory fusion pore. Under sympathetic tone, basal synaptic excitation drives chromaffin cells to selectively secrete modest levels of catecholamine through a restricted secretory fusion pore. In contrast, elevated sympathetic activity, experienced under stress, results in fusion pore expansion to evoke maximal catecholamine release and to facilitate release of co-packaged peptide transmitters. Therefore, fusion pore expansion is a key control point for the activation of the sympatho-adrenal stress response. Despite the physiological importance of this process, the molecular mechanism by which it is regulated remains unclear. Here we employ fluorescence imaging with electrophysiological, and electrochemical-based approaches to investigate the role of dynamin I in the regulation of activity-mediated fusion pore expansion in mouse adrenal chromaffin cells. We show that under elevated stimulation, dynamin I is dephosphorylated at Ser-774 by calcineurin. We also demonstrate that disruption of dynamin I-syndapin binding, an association regulated by calcineurin-dependent dynamin dephosphorylation, limits fusion pore expansion. Lastly, we show that perturbation of N-WASP function (a syndapin substrate) limits activity-mediated fusion pore expansion. Our results suggest that fusion pore expansion is regulated by a calcineurin-dependent dephosphorylation of dynamin I. Dephosphorylated dynamin I acts via a syndapin/N-WASP signaling cascade to mediate pore expansion.

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Past, Present and Future of Human Chromaffin Cells: Role in Physiology and Therapeutics

Cited by 15 publications

References 109 publications

The Effects of Nanomaterials as Endocrine Disruptors

The Effects of Nanomaterials as Endocrine Disruptors

Sympathetic Nervous System Signaling in Heart Failure and Cardiac Aging

Activity-Dependent Fusion Pore Expansion Regulated by a Calcineurin-Dependent Dynamin-Syndapin Pathway in Mouse Adrenal Chromaffin Cells

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