Chromaffin Cells of the Adrenal Medulla: Physiology, Pharmacology, and Disease

Carbone, Emilio; Borges, Ricardo; Eiden, Lee E.; Garcı́a, Antonio G.; Hernández‐Cruz, Arturo

doi:10.1002/cphy.c190003

Cited by 62 publications

(52 citation statements)

References 665 publications

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“…Notice that a decreased density of Nav channels together with an increased inward Ca influx boost MCCs to fire in burst and generate further Ca entry [21,41,95], thus sustaining high levels of intracellular Ca .…”

Section: +mentioning

confidence: 99%

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Cav1.2 channelopathies causing autism: new hallmarks on Timothy syndrome

Marcantoni¹,

Calorio²,

Hidişoğlu

et al. 2020

Pflugers Arch - Eur J Physiol

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Section: +mentioning

confidence: 99%

“…Cav1.2 (encoded by the gene CACNA1C) is an L-type calcium channel with broad tissue expression profile, including cardiac and neuronal tissues, smooth muscle, pituitary, and adrenal glands [21,23,30,103]. Cav1.2 channels open upon cell depolarization to enable Ca influx and initiate intracellular Camediated signaling [44,47].…”

mentioning

confidence: 99%

Cav1.2 channelopathies causing autism: new hallmarks on Timothy syndrome

Marcantoni¹,

Calorio²,

Hidişoğlu

et al. 2020

Pflugers Arch - Eur J Physiol

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“…Continuous exposure to stress enhances the progression of cancers, and this is partly mediated by NE and epinephrine released during increased sympathetic nervous activity as part of the body's fight-or-flight stress response [39]. During stress, NE is locally secreted from nerve endings in various tissues and then into the blood, while epinephrine is secreted from the adrenal medulla [40][41][42]. In many types of tumors, NE, epinephrine, and activation of adrenergic receptors are involved in tumorigenesis, cancer survival, proliferation, angiogenesis, tumor progression, and metastasis through adrenergic receptor signaling-coupled intracellular molecular pathways [43,44] or immunosuppression in the tumor microenvironment [45,46].…”

Section: Discussionmentioning

confidence: 99%

Norepinephrine-stimulated HSCs secrete sFRP1 to promote HCC progression following chronic stress via augmentation of a Wnt16B/β-catenin positive feedback loop

Lin

Liu

Hsu

et al. 2020

J Exp Clin Cancer Res

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Background: Sustained adrenergic signaling secondary to chronic stress promotes cancer progression; however, the underlying mechanisms for this phenomenon remain unclear. Hepatocellular carcinoma (HCC) frequently develops within fibrotic livers rich in activated hepatic stellate cells (HSCs). Here, we examined whether the stress hormone norepinephrine (NE) could accelerate HCC progression by modulating HSCs activities.Methods: HCC cells were exposed to conditioned medium (CM) from NE-stimulated HSCs. The changes in cell migration and invasion, epithelial-mesenchymal transition, parameters of cell proliferation, and levels of cancer stem cell markers were analyzed. Moreover, the in vivo tumor progression of HCC cells inoculated with HSCs was studied in nude mice subjected to chronic restraint stress.Results: CM from NE-treated HSCs significantly promoted cell migration and invasion, epithelial-mesenchymal transition (EMT), and expression of cell proliferation-related genes and cancer stem cell markers in HCC cells. These protumoral effects were markedly reduced by depleting secreted frizzled related protein 1 (sFRP1) in CM. The pro-tumoral functions of sFRP1 were dependent on β-catenin activation, and sFRP1 augmented the binding of Wnt16B to its receptor FZD7, resulting in enhanced β-catenin activity. Additionally, sFRP1 enhanced Wnt16B expression, reinforcing an autocrine feedback loop of Wnt16B/β-catenin signaling. The expression of sFRP1 in HSCs promoted HCC progression in an in vivo model under chronic restraint stress, which was largely attenuated by sFRP1 knockdown. Conclusions: We identify a new mechanism by which chronic stress promotes HCC progression. In this model, NE activates HSCs to secrete sFRP1, which cooperates with a Wnt16B/β-catenin positive feedback loop. Our findings have therapeutic implications for the treatment of chronic stress-promoted HCC progression.

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“…Adrenal medulla chromaffin cells (CCs) are invaluable cell models for neurosecretion studies [5]. Significant differences in Ca 2+ dynamics and exocytosis exist in CCs from several mammalian species (bovine, rat, guinea pig, cat, human) [7].…”

mentioning

confidence: 99%

“…Significant differences in Ca 2+ dynamics and exocytosis exist in CCs from several mammalian species (bovine, rat, guinea pig, cat, human) [7]. Nonetheless, the interest in mouse CCs (MCCs) increased disproportionally after the advent of transgenic mouse models to explore, from the complexities of Ca 2+ signaling and exocytosis to alterations of Ca 2+ homeostasis in neurodegenerative diseases [5].…”

mentioning

confidence: 99%

Reversible interruption of ER Ca2+ uptake inversely affects ACh-elicited exocytosis in mouse and bovine chromaffin cells

Hernández‐Cruz

2020

Pflugers Arch - Eur J Physiol

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Chromaffin Cells of the Adrenal Medulla: Physiology, Pharmacology, and Disease

Cited by 62 publications

References 665 publications

Cav1.2 channelopathies causing autism: new hallmarks on Timothy syndrome

Cav1.2 channelopathies causing autism: new hallmarks on Timothy syndrome

Norepinephrine-stimulated HSCs secrete sFRP1 to promote HCC progression following chronic stress via augmentation of a Wnt16B/β-catenin positive feedback loop

Reversible interruption of ER Ca2+ uptake inversely affects ACh-elicited exocytosis in mouse and bovine chromaffin cells

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