Angiotensin II AT1 receptors and Na+/K+ ATPase in human umbilical vein endothelial cells

Muscella, Antonella; Marsigliante, Santo; Carluccio, Maria Annunziata; Vinson, G. P.; Storelli, Carlo

doi:10.1677/joe.0.1550587

Cited by 16 publications

(10 citation statements)

References 32 publications

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“…Unless specifically stated otherwise, HUVEC were pre‐incubated for 30 min with 10 − 9 –10 − 6 mol/L Ang‐(1–7) alone (Sigma‐Aldrich, St Louis, MO, USA) or 10 − 6 mol/L Ang‐(1–7) plus 10 − 6 mol/L A‐779 (Bachem, Torrance, CA, USA), an antagonist of the Mas receptor, before being incubated with 10 − 6 mol/L AngII (10 − 6 mol/L; Sigma‐Aldrich) for a further 24 h. Cells were then washed three times with PBS before analysis. The concentration of AngII used in the present study was chosen on the basis of previous reports . The control group consisted of HUVEC that had not been subjected to any treatment.…”

Section: Methodsmentioning

confidence: 99%

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Angiotensin‐(1–7) treatment ameliorates angiotensin II‐induced apoptosis of human umbilical vein endothelial cells

Yang

Bian

Zhang

et al. 2012

Clin Exp Pharma Physio

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Angiotensin (Ang)-(1-7), a metabolite of AngI and AngII, is a counter-regulatory mediator of AngII. In the present study, we investigated the effects of Ang-(1-7) on AngII-induced apoptosis in human umbilical vein endothelial cells (HUVEC). To this end, HUVEC were pretreated with 10(-9), 10(-8), 10(-7) or 10(-6) mol/L Ang-(1-7) at for 30 min before being stimulated with 10(-6) mol/L Ang-II for another 24 h. Acridine orange/ethidium bromide and propidium iodide staining were used to analyse the effects of Ang-(1-7) on AngII-induced apoptosis. Alone, 10(-6) mol/L Ang-(1-7) had no effect on the apoptosis of HUVEC following exposure of cells for 30 min, whereas AngII (10(-6) mol/L, 24 h) significantly enhanced the number of apoptotic cells (P < 0.01). The AngII-induced apoptosis of HUVEC was suppressed by 10(-9)-10(-6) mol/L Ang-(1-7). The anti-apoptotic effects of Ang-(1-7) were almost completely abolished by A-779 (10(-6) mol/L, 30 min), a specific Mas receptor antagonist. In addition, Ang-(1-7) inhibited AngII-induced accumulation of cleaved caspase 3 and enhanced the expression of the anti-apoptotic factor Bcl-2 at both the mRNA and protein levels. Angiotensin II upregulated the expression of lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1), which is involved in endothelial apoptosis, at both the mRNA and protein levels. This effect was blocked by Ang-(1-7) in a concentration-dependent manner, although A-779 almost completely reversed Ang-(1-7)-mediated inhibition of AngII-induced upregulation of LOX-1. Silencing of LOX-1 using short interference RNA enhanced the protective effects of Ang-(1-7) against AngII-induced apoptosis in HUVEC. Together, the results suggest that Ang-(1-7) ameliorates AngII-induced apoptosis of HUVEC at least in part by suppressing LOX-1 expression.

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Section: Methodsmentioning

confidence: 99%

“…The concentration of AngII used in the present study was chosen on the basis of previous reports. 19,20 The control group consisted of HUVEC that had not been subjected to any treatment.…”

Section: Cell Treatmentsmentioning

confidence: 99%

Angiotensin‐(1–7) treatment ameliorates angiotensin II‐induced apoptosis of human umbilical vein endothelial cells

Yang

Bian

Zhang

et al. 2012

Clin Exp Pharma Physio

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“…In view of the central role of Na ϩ ,K ϩ -ATPase in the control of astroglial function and in neuron-astrocyte interactions, it is important to identify the factors regulating this enzymatic activity. In other tissues, Na ϩ ,K ϩ -ATPase activity is modulated by several hormones, including Ang II (Orlov et al, 1992;Simmons and Winegrad, 1992;Aperia et al, 1994;Muscella et al, 1997;Bharatula et al, 1998;Hussain et al, 1998). The present study was aimed at investigating whether Ang II also regulates the activity of this transporter in cultured rat astrocytes.…”

mentioning

confidence: 97%

Angiotensin II Modulates the Activity of Na⁺,K⁺‐ATPase in Cultured Rat Astrocytes via the AT1 Receptor and Protein Kinase C‐δ Activation

Muscella

Aloisi

Marsigliante

et al. 2000

Journal of Neurochemistry

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In astrocytes the activity of the Na+,K(+)-ATPase pump maintains an inwardly directed electrochemical sodium gradient used by the Na+-dependent transporters and regulates the extracellular K+ concentration essential for neuronal excitability. We show here that incubation of cultured rat astrocytes with angiotensin II (Ang II) modulates Na+,K(+)-ATPase activity, in a dose- and time-dependent manner. Na+,K(+)-ATPase activation was mediated by binding of Ang II to AT1 receptors as it was completely blocked by DuP 753, a specific AT1 receptor subtype antagonist. Stimulation of Na+,K(+)-ATPase activity by Ang II was dependent on protein kinase C (PKC) activation because PKC antagonists abolished the inducing effect of Ang II and the PKC activator phorbol 12-myristate 13-acetate enhanced transporter activity. Ang II stimulated translocation of PKC-delta but not that of other PKC isoforms from the cytosol to the plasma membrane. These results indicate that the activity of Na+,K(+)-ATPase in astrocytes is increased by physiological concentrations of Ang II and that the AT1 receptor subtype mediates the Na+,K(+)-ATPase response to Ang II via PKC-delta activation.

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“…the expression of endothelial cell specific markers such as von Willebrand factor and an endothelial specific adhesion molecule, CD31, expression of receptors for growth factors, cytokines, vasoactive ligands, and specific signaling pathways for vascular endothelial growth factor (VEGF), fibroblast growth factor (FGF), transforming growth factor-β, tumor necrosis factor (TNF)-α and angiotensin II (6)(7)(8)(9). Human umbilical vein endothelial cells (HUVECs) have provided a critical in vitro model for major breakthroughs in molecular medicine including seminal insights into cellular and molecular events in the pathophysiology of atherosclerosis and plaque formation, and mechanisms for the control of angiogenesis or neovascularization in response to hypoxia and inflammation in tumors, ischemic tissue, and in embryogenesis (10)(11)(12).…”

mentioning

confidence: 99%

Human umbilical vein endothelial cells and human dermal microvascular endothelial cells offer new insights into the relationship between lipid metabolism and angiogenesis

et al. 2006

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Human umbilical vein endothelial cells (HUVECs) have played a major role as a model system for the study of the regulation of endothelial cell function and the role of the endothelium in the response of the blood vessel wall to stretch, shear forces, and the development of atherosclerotic plaques and angiogenesis. Here, we use HUVECs and human microvascular endothelial cells to study the role of the HMG-CoA reductase inhibitor, simvastatin, and the small GTP-binding protein Rho in the regulation of angiogenesis. Simvastatin inhibited angiogenesis in response to FGF-2 in the corneal pocket assay of the mouse and in vascular endothelial growth factor (VEGF)-stimulated angiogenesis in the chick chorioallontoic membrane. Furthermore, simvastatin inhibited VEGF-stimulated tube formation by human dermal microvascular endothelial cells and the formation of honeycomb-like structures by HUVECs. The effect was dose-dependent and was not secondary to apoptosis. Geranylgeranyl-pyrophosphate (GGPP), a product of the cholesterol metabolic pathway that serves as a substrate for the posttranslational lipidation of RhoA, was required for membrane localization, but not farnesylpyrophosphate (FPP), the substrate for the lipidation of Ras. Furthermore, GGTI, a specific inhibitor of GGPP, mimicked the effect of simvastatin of tube formation and the formation of honeycombs whereas FTI, a specific inhibitor of the farnesylation of Ras, had no effect. Adenoviral expression of a DN-RhoA mutant mimicked the effect of simvastatin on tube formation and the formation of honeycombs, whereas a dominant activating mutant of RhoA reversed the effect of simvastatin on tube formation. Finally, simvastatin interfered with the membrane localization of RhoA with a dose-dependence similar to that for the inhibition of tube formation. Simvastatin also inhibited the VEGFstimulated phosphorylation of the VEGF receptor KDR, and the tyrosine kinase FAK, which plays a role in cell migration. These data demonstrate that simvastatin interfered with angiogenesis via the inhibition of RhoA. Data supporting a role for angiogenesis in the development and growth of atherosclerotic plaques suggest that this antiangiogenic effect of Statins might prevent the progression of atherosclerosis via the inhibition of plaque angiogenesis.

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Angiotensin II AT1 receptors and Na+/K+ ATPase in human umbilical vein endothelial cells

Abstract: Abstract

Cited by 16 publications

References 32 publications

Angiotensin‐(1–7) treatment ameliorates angiotensin II‐induced apoptosis of human umbilical vein endothelial cells

Angiotensin‐(1–7) treatment ameliorates angiotensin II‐induced apoptosis of human umbilical vein endothelial cells

Angiotensin II Modulates the Activity of Na⁺,K⁺‐ATPase in Cultured Rat Astrocytes via the AT1 Receptor and Protein Kinase C‐δ Activation

Human umbilical vein endothelial cells and human dermal microvascular endothelial cells offer new insights into the relationship between lipid metabolism and angiogenesis

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Angiotensin II AT1 receptors and Na+/K+ ATPase in human umbilical vein endothelial cells

Abstract: Abstract

Cited by 16 publications

References 32 publications

Angiotensin‐(1–7) treatment ameliorates angiotensin II‐induced apoptosis of human umbilical vein endothelial cells

Angiotensin‐(1–7) treatment ameliorates angiotensin II‐induced apoptosis of human umbilical vein endothelial cells

Angiotensin II Modulates the Activity of Na+,K+‐ATPase in Cultured Rat Astrocytes via the AT1 Receptor and Protein Kinase C‐δ Activation

Human umbilical vein endothelial cells and human dermal microvascular endothelial cells offer new insights into the relationship between lipid metabolism and angiogenesis

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Angiotensin II Modulates the Activity of Na⁺,K⁺‐ATPase in Cultured Rat Astrocytes via the AT1 Receptor and Protein Kinase C‐δ Activation