Ca2+ removal mechanisms in freshly isolated rabbit aortic endothelial cells

Wang, X; Reznick, S; Li, P; Liang, Willmann; Breemen, Cornelis van

doi:10.1016/s0143-4160(02)00075-1

Cited by 35 publications

(33 citation statements)

References 21 publications

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“…Images of hVMFs exposed to 340-and 380-nm UV light in 1-second intervals were recorded and the fluorescence ratio (F 340 /F 380 ) of individual cells was analyzed using Northern Eclipse software (Empix, Toronto, ON ] i instead. 10,11) All experiments were performed at room temperature (23°C).…”

Section: Methodsmentioning

confidence: 99%

P2Y2 Receptor-Mediated Ca2+ Signaling and Spontaneous Ca2+ Releases in Human Valvular Myofibroblasts

et al. 2008

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Section: Methodsmentioning

confidence: 99%

P2Y2 Receptor-Mediated Ca2+ Signaling and Spontaneous Ca2+ Releases in Human Valvular Myofibroblasts

et al. 2008

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“…Cytoplasmic calcium homeostasis is largely regulated by the plasma membrane Ca 2+ ATPase (PMCA), the endoplasmic Ca 2+ ATPase (SERCA), and the plasmalemmal Na + /Ca 2+ exchanger (NCX) [29]. Inhibition of PMCA with La 3+ , or SER-CA with thapsigargin (for ≥30 min following the initial NO stimulation produced by delayed cytoplasmic Ca 2+ removal) did not affect the D-glucose-induced endothelial NO response.…”

Section: Involvement Of Ca2+ Transporters In Glucose-mediated Enos Acmentioning

confidence: 96%

Acute effects of glucose and insulin on vascular endothelium

et al. 2004

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Aims/hypothesis. Chronic exposure to high concentrations of glucose has consistently been demonstrated to impair endothelium-dependent, nitric oxide (NO)-mediated vasodilation. In contrast, several clinical investigations have reported that acute exposure to high glucose, alone or in combination with insulin, triggers vasodilation. The aim of this study was to examine whether elevated glucose itself stimulates endothelial NO formation or enhances insulin-mediated endothelial NO release. Methods. We measured NO release and vessel tone ex vivo in porcine coronary conduit arteries (PCAs). Intracellular Ca 2+ was monitored in porcine aortic endothelial cells (PAECs) by fura-2 fluorescence. Expression of the Na + /glucose cotransporter-1 (SGLT-1) was assayed in PAECs and PCA endothelium by RT-PCR. Results. Stimulation of PCAs with D-glucose, but not the osmotic control L-glucose, induced a transient increase in NO release (EC 50 ≈10 mmol/l), mediated by a rise in intracellular Ca 2+ levels due to an influx from the extracellular space. This effect was abolished by inhibitors of the plasmalemmal Na + /Ca 2+ exchanger (dichlorobenzamil) and the SGLT-1 (phlorizin), which was found to be expressed in aortic and coronary endothelium. Alone, D-glucose did not relax PCA, but did augment the effect of insulin on NO release and vasodilation. Conclusions/interpretation. An increased supply of extracellular D-glucose appears to enhance the activity of the endothelial isoform of nitric oxide synthase by increasing intracellular Na + concentrations via SGLT-1, which in turn stimulates an extracellular Ca 2+ influx through the Na + /Ca 2+ exchanger. This mechanism may be responsible for glucose-enhanced, insulin-dependent increases in tissue perfusion (including coronary blood-flow), thus accelerating glucose extraction from the blood circulation to limit the adverse vascular effects of prolonged hyperglycaemia.

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“…The return of [Ca 2C ] c to control values was shown to be related to the activation of the PMCA pump and NCX activation, which are widely reported to restore the basal intracellular Ca 2C levels in endothelial cells (Moccia et al 2002, Wang et al 2002. Hence, in PCAEC and HCAEC cultured in Na C -free medium, the decay phase of the gastrin-17-evoked Ca 2C transient was significantly longer.…”

Section: Figurementioning

confidence: 82%

“…Also, the release of intracellular Ca 2C coupled to subsequent Ca 2C entry (Putney 1990), known as 'capacitative Ca 2C entry', is a mechanism widely reported to affect Ca 2C homeostasis in response to both receptor-mediated stimuli (Putney 1990, Schilling et al 1992, Fasolato & Nilius 1998 and receptor-independent emptying of intracellular stores by agents such as thapsigargin, cyclovirobuxine D and urocortin II (Putney 1990, Schilling et al 1992, Fasolato & Nilius 1998, Grossini et al 2005, 2010. In addition, the restoration of basal intracellular Ca 2C levels would play an important role by the activation of the plasma membrane Ca 2C -ATPase (PMCA) pump and of Na C /Ca 2C exchanger (NCX; Moccia et al 2002, Wang et al 2002. Changes of [Ca 2C ] c have been reported to be also crucial for the response of gastrointestinal cells to CCK receptor agonists.…”

Section: Changes Of Cytosolic Camentioning

confidence: 99%

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Calcium handling in porcine coronary endothelial cells by gastrin-17

Grossini

Molinari

Sigaudo

et al. 2013

Journal of Molecular Endocrinology

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In porcine coronary artery endothelial cells (PCAEC), gastrin-17 has recently been found to increase nitric oxide (NO) production by the endothelial NO synthase (eNOS) isoform through cholecystokinin 1/2 (CCK1/2) receptors and the involvement of protein kinase A (PKA), PKC and the b 2 -adrenoreceptor-related pathway. As eNOS is the Ca 2C -dependent isoform of the enzyme, we aimed to examine the effects of gastrin-17 on Ca 2C movements.Thus, experiments were performed in Fura-2-acetoxymethyl-ester-loaded PCAEC, where changes of cytosolic Ca 2C ([Ca 2C ] c ) caused by gastrin-17 were analysed and compared with those of CCK receptors and b 2 -adrenoreceptors agonists/antagonists. In addition, some experiments were performed by stimulating cells with gastrin-17 in the presence or absence of cAMP/PKA activator/inhibitor and of phospholipase C (PLC) and Ca 2C-calmodulin dependent protein kinase II (CaMKII) blockers. The results have shown that gastrin-17 can promote a transient increase in [Ca 2C ] c mainly originating from an intracellular pool sensitive to thapsigargin and from the extracellular space. In addition, the response of cells to gastrin-17 was increased by the adenylyl cyclase activator and the b 2 -adrenoreceptor agonists and affected mainly by the CCK2 receptor agonists/antagonists. Moreover, the effects of gastrin-17 were prevented by b 2 -adrenoreceptors and CaMKII blockers and the adenylyl cyclase/PKA and PLC inhibitors. Finally, in PCAEC cultured in Na C -free medium or loaded with the plasma membrane Ca 2C pump inhibitor, the gastrin-17-evoked Ca 2C transient was long lasting.In conclusion, this study shows that gastrin-17 affected intracellular Ca 2C homeostasis in PCAEC by both promoting a discharge of an intracellular pool and by interfering with the operation of store-dependent channels through mainly CCK2 receptors and PKA/PLC-and CaMKII-related signalling downstream of b 2 -adrenoreceptor stimulation.

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Ca2+ removal mechanisms in freshly isolated rabbit aortic endothelial cells

Cited by 35 publications

References 21 publications

P2Y2 Receptor-Mediated Ca2+ Signaling and Spontaneous Ca2+ Releases in Human Valvular Myofibroblasts

P2Y2 Receptor-Mediated Ca2+ Signaling and Spontaneous Ca2+ Releases in Human Valvular Myofibroblasts

Acute effects of glucose and insulin on vascular endothelium

Calcium handling in porcine coronary endothelial cells by gastrin-17

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