Signalling pathways evoked by α1-adrenoceptors in human melanoma cells

Scarparo, Ana Cristina; Visconti, Maria Aparecida; Castrucci, Ana Maria de Lauro

doi:10.1002/cbf.1309

Cited by 14 publications

(11 citation statements)

References 59 publications

(73 reference statements)

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“…To evaluate the contribution of MAPK, which is normally related to signal transduction coupled to α 1 ‐adrenoceptors and also linked to noradrenaline‐induced stimulation of sodium reabsorption in the kidney and vascular tissues ( Liu and Gesek, 2001 ; Hutchinson and Bengtsson, 2005 ; Scarparo et al , 2006 ), we used specific inhibitors for MAPK/extracellular signal‐regulated kinase kinase (MEK) and p38 MAPK. Pretreatment of cells for 15 min with the MEK 1 inhibitor PD 098059 abolished the phenylephrine‐induced stimulation of Cl − /HCO 3 − exchanger activity in WKY PTE cells, but not in SHR PTE cells (Figure 5).…”

Section: Resultsmentioning

confidence: 99%

Oxidative stress and α₁‐adrenoceptor‐mediated stimulation of the Cl⁻/HCO₃⁻ exchanger in immortalized SHR proximal tubular epithelial cells

Simão¹,

Fraga²,

José³

et al. 2008

British J Pharmacology

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Background and purpose: This study evaluated the signalling coupled to the a 1 -adrenoceptor-induced stimulation of the Cl À / HCO 3 À exchanger in hypertension. Experimental approach: The Na þ -independent HCO 3 À transport system activity was assayed as the initial rate of pH i recovery after an alkaline load (CO 2 /HCO 3 removal) in immortalized renal proximal tubular epithelial cells from spontaneously hypertensive rat (SHR) and their normotensive control (Wistar Kyoto rat; WKY). Key results: Noradrenaline increased Cl À /HCO 3 À exchanger activity with EC 50 values of 0.6 and 5.3 mM in SHR and WKY cells, respectively. These effects were abolished by prazosin, but not by yohimbine. Phenylephrine increased Cl À /HCO 3 À exchanger activity in SHR and WKY cells (EC 50 of 2.6 and 4.9 mM, respectively). Phenylephrine-mediated increase in Cl À /HCO 3 À exchanger activity in WKY and SHR cells was inhibited by protein kinase C (PKC), MAPK/ERK kinase (MEK) and p38 mitogen-activated protein kinase (p38 MAPK) inhibitors. The expression of a 1A -and a 1B -adrenoceptors was identical in WKY and SHR cells. SHR cells generated more H 2 O 2 than WKY cells. In SHR cells, the NADPH oxidase inhibitor apocynin reduced their increased ability to generate H 2 O 2 and abolished their hypersensitivity to phenylephrine, but failed to affect basal Cl À /HCO 3 À exchanger activity. H 2 O 2 -dependent stimulation of Cl À /HCO 3 À exchange activity was significantly higher in SHR than in WKY cells. Conclusions and implications: Differences between WKY and SHR cells on their sensitivity to a 1 -adrenoceptor stimulation did not correlate with the abundance of a 1A -and a 1B -adrenoceptors and may be related to the increased generation of H 2 O 2 , which may amplify the response downstream of a 1 -adrenoceptor activation.

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Section: Resultsmentioning

confidence: 99%

Oxidative stress and α₁‐adrenoceptor‐mediated stimulation of the Cl⁻/HCO₃⁻ exchanger in immortalized SHR proximal tubular epithelial cells

Simão¹,

Fraga²,

José³

et al. 2008

British J Pharmacology

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“…The administration of an alpha1-adrenergic agonist such as phenylephrine thereby induces decreased proliferation and increased tyrosinase activity while an alpha1-adrenergic antagonist such as prazosine blocks these activities. It therefore seems that alpha1-adrenoceptors, expressed by melanoma cells, have a low affinity for catecholamines and exert a marginal role in tumor growth and invasion [34, 35]. …”

Section: Melanoma and Stressmentioning

confidence: 99%

Stress as a Possible Mechanism in Melanoma Progression

Sanzo

Colucci

Arunachalam

et al. 2010

Dermatology Research and Practice

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The incidence of melanoma, the most aggressive type of cutaneous malignant tumor, is currently on the rise. Treatment in advanced stages is still unsuccessful compared with other malignant tumors, thus it is important to indentify the key mechanisms responsible for melanoma progression and metastasis. Genetic and molecular components, in particular, that are up- or downregulated in melanoma cells, affect the invasive potential of melanoma. Another possible important cofactor highlighted by recent studies is chronic stress, involving environmental and psychological factors, which can be an important cofactor in not only cancer progression in general but also in melanoma spreading. The negative effects of chronic stress have been evaluated epidemiologically in patients with breast and prostate cancer. In particular, the effects of stress mediators, namely, catecholamines have been studied on various human malignancies, including melanoma and have highlighted a significant increase of progression-related molecules. As such, this could be the starting point for a new approach in the treatment of advanced melanoma, in which the negative effects of stress are reduced or blocked.

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“…Although previous studies have revealed the presence of alpha1adrenoceptor in human melanoma cells, they seem to have a reduced affinity for adrenergic agonists and their effect on tumor growth and invasiveness is still unclear (41,42).…”

Section: Discussionmentioning

confidence: 98%

Catecholamines Increase in Vitro Proliferation of Murine B16F10 Melanoma Cells

Căruntu¹

2014

Acta Endo (Buc)

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Context.Melanoma is the most aggressive skin cancer, with significant morbidity and mortality, and one factor that may influence the course of disease is stress.Objective. Our aim was to evaluate the effect of corticosterone, norepinephrine, epinephrine on murine B16F10 melanoma cells in vitro proliferation.Methods. B16F10 melanoma cells were treated with different concentrations of tested hormones. The proliferative capacity of melanoma cells was quantified by MTS assay and the cell viability was quantified as membrane integrity evaluation measured by lactate dehydrogenase (LDH) release.Results. B16F10 cells treated with corticosterone showed no significant changes. In contrast, norepinephrine exposure stimulated the cell proliferation (P = 0.0003). Treatment with 1 µM norepinephrine induced the highest increase in cell proliferation (OD 492 = 0.27 ± 0.02) statistically significant to both control (OD 492 = 0.17 ± 0.01; p = 0.0003), 10 nM norepinephrine (OD 492 = 0.16 ± 0.00; p = 0.0004) and 100 nM norepinephrine (OD 492 = 0.19 ± 0.01; p = 0.002). Likewise, treatment with epinephrine increased cell proliferation (p = 0.0004). Exposure to 5 µm epinephrine induced a stimulation of cell proliferation (OD 492 = 0.28 ± 0.02) significantly higher compared to controls (OD 492 = 0.17 ± 0.01; p = 0.0004), 50 nM epinephrine (OD 492 = 0.17 ± 0.00; p = 0.001) and 500 nM epinephrine (OD 492 = 0.173 ± 0.00; p = 0.001). Conclusions.Our results may open new perspectives concerning the link between stress hormones and melanoma, emphasizing a direct stimulating in vitro effect induced by catecholamines on melanoma B16F10 cells proliferation.

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Signalling pathways evoked by α1-adrenoceptors in human melanoma cells

Cited by 14 publications

References 59 publications

Oxidative stress and α₁‐adrenoceptor‐mediated stimulation of the Cl⁻/HCO₃⁻ exchanger in immortalized SHR proximal tubular epithelial cells

Oxidative stress and α₁‐adrenoceptor‐mediated stimulation of the Cl⁻/HCO₃⁻ exchanger in immortalized SHR proximal tubular epithelial cells

Stress as a Possible Mechanism in Melanoma Progression

Catecholamines Increase in Vitro Proliferation of Murine B16F10 Melanoma Cells

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Signalling pathways evoked by α1-adrenoceptors in human melanoma cells

Cited by 14 publications

References 59 publications

Oxidative stress and α1‐adrenoceptor‐mediated stimulation of the Cl−/HCO3− exchanger in immortalized SHR proximal tubular epithelial cells

Oxidative stress and α1‐adrenoceptor‐mediated stimulation of the Cl−/HCO3− exchanger in immortalized SHR proximal tubular epithelial cells

Stress as a Possible Mechanism in Melanoma Progression

Catecholamines Increase in Vitro Proliferation of Murine B16F10 Melanoma Cells

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Oxidative stress and α₁‐adrenoceptor‐mediated stimulation of the Cl⁻/HCO₃⁻ exchanger in immortalized SHR proximal tubular epithelial cells

Oxidative stress and α₁‐adrenoceptor‐mediated stimulation of the Cl⁻/HCO₃⁻ exchanger in immortalized SHR proximal tubular epithelial cells