Dynamic regulation of [Ca2+]iby plasma membrane Ca2+-ATPase and Na+/Ca2+exchange during capacitative Ca2+entry in bovine vascular endothelial cells

Sedova, Marina; Blatter, Lothar A.

doi:10.1054/ceca.1999.0036

Cited by 84 publications

(88 citation statements)

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“…These blockades did not significantly affect BK-induced NO production by adjacent IICRintact cells. Thus, Ca i elevation, consistent with the results of previous studies (16,55,56).…”

Section: Discussionsupporting

confidence: 92%

Autocrine Action and Its Underlying Mechanism of Nitric Oxide on Intracellular Ca2+ Homeostasis in Vascular Endothelial Cells

Chen¹,

Wang²,

Wang³

et al. 2000

Journal of Biological Chemistry

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“…These blockades did not significantly affect BK-induced NO production by adjacent IICRintact cells. Thus, Ca i elevation, consistent with the results of previous studies (16,55,56).…”

Section: Discussionsupporting

confidence: 92%

Autocrine Action and Its Underlying Mechanism of Nitric Oxide on Intracellular Ca2+ Homeostasis in Vascular Endothelial Cells

Chen¹,

Wang²,

Wang³

et al. 2000

Journal of Biological Chemistry

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“…Na ϩ /Ca 2ϩ -free PSS was used throughout the experiment to prevent the Na ϩ /Ca 2ϩ exchanger from contributing to Ca 2ϩ efflux (27,29). Hence the rate of decline in [Ca 2ϩ ] i was predominately a measure of PMCA-mediated free intracellular Ca 2ϩ efflux.…”

Section: Plasma Membrane Ca 2ϩ -Atpase Inhibition In Mcf-7 Cellsmentioning

confidence: 99%

“…In this equation, F t equals the fluorescence reading at each time point (t), and F 0 represents initial fluorescence at t ϭ 0 (30). For each well, where peak [Ca 2ϩ ] i was obtained within 90.5 s following the addition of ionomycin, the fluorescence data corresponding to the 60 s after and including the peak ⌬F/F was fitted to a monoexponential curve as a measure of the rate of PMCA-mediated free intracellular Ca 2ϩ efflux (29). Statistical Analyses-All data points are presented as means Ϯ S.D., unless otherwise stated, for the number of replicates (n) indicated.…”

Section: Plasma Membrane Ca 2ϩ -Atpase Inhibition In Mcf-7 Cellsmentioning

confidence: 99%

Antisense-mediated Inhibition of the Plasma Membrane Calcium-ATPase Suppresses Proliferation of MCF-7 Cells

Lee

Robinson

Holman

et al. 2005

Journal of Biological Chemistry

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Alterations in Ca2؉ signaling may contribute to tumorigenesis and the mechanism of action of some anticancer drugs. The plasma membrane calcium-ATPase (PMCA) is a crucial controller of intracellular Ca 2؉ signaling. Altered PMCA expression occurs in the mammary gland during lactation and in breast cancer cell lines. Despite this, the consequences of PMCA inhibition in breast cancer cell lines have not been investigated. In this work, we used Tet-off PMCA antisense-expressing MCF-7 cells to assess the effects of PMCA inhibition in a human breast cancer cell line. At a level of PMCA inhibition that did not completely prevent PMCA-mediated Ca 2؉ efflux and did not induce cell death, a dramatic inhibition of cellular proliferation was observed. Fluorescence-activated cell sorting analysis indicated that PMCA antisense involves changes in cell cycle kinetics but not cell cycle arrest. We concluded that modulation of PMCA has important effects in regulating the proliferation of human breast cancer MCF-7 cells.

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“…These proteins are localised in the plasmalemmal caveolae in close proximity to eNOS and participate in the control of sub-plasmalemmal intracellular Ca 2+ , which is of particular importance for modulation of eNOS activity [34,35]. The high affinity/low capacity PMCA is the principal Ca 2+ removal system in vascular endothelium [36]. However, failure of the PMCA-(and capacitative Ca 2+ entry-) inhibitor La 3+ to diminish D-glucose-mediated NO formation suggests that intracellular Ca 2+ clearance by PMCA is not involved in glucose-dependent eNOS activation.…”

Section: Additive Effects Of D-glucose and Insulin On Nitric Oxide Fomentioning

confidence: 99%

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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Dynamic regulation of [Ca2+]iby plasma membrane Ca2+-ATPase and Na+/Ca2+exchange during capacitative Ca2+entry in bovine vascular endothelial cells

Cited by 84 publications

References 0 publications

Autocrine Action and Its Underlying Mechanism of Nitric Oxide on Intracellular Ca2+ Homeostasis in Vascular Endothelial Cells

Autocrine Action and Its Underlying Mechanism of Nitric Oxide on Intracellular Ca2+ Homeostasis in Vascular Endothelial Cells

Antisense-mediated Inhibition of the Plasma Membrane Calcium-ATPase Suppresses Proliferation of MCF-7 Cells

Acute effects of glucose and insulin on vascular endothelium

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