Vectorial Ca2+ release via ryanodine receptors contributes to Ca2+ extrusion from freshly isolated rabbit aortic endothelial cells

Liang, Willmann; Buluç, M.; Breemen, Cornelis van; Wang, Xiaodong

doi:10.1016/j.ceca.2004.04.003

Cited by 24 publications

(20 citation statements)

References 26 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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“…The SCCU enables a functional coupling between RyRs expressed on superficial ER and plasmalemmal NCX, so that Ca 2+ released from RyRs is vectorially pumped out by NCX without affecting [Ca 2+ ]i. Under these conditions, RyR contribution to endothelial Ca 2+ signaling may be appreciated only upon NCX inhibition [133,138,139] or by monitoring the local activation of large conductance Ca 2+ -dependent K + channels [140,141] . Besides CICR, RyRs may be stimulated by cADPr [10] , a second messenger that can be generated in response to either agonist stimulation [142] or oxidative stress through the synthesis of H2O2 [143,144] .…”

Section: Ryrs and Cadprmentioning

confidence: 99%

“…The sequence of events leading to removal of cytosolic Ca 2+ may be different in ECs from different vascular beds and three main Ca 2+ -buffering pathways have hitherto been identified. (1) In-series arrangement of RyRs and NCX and of SERCA and RyRs [139,345] : according to this model, that has been described in rabbit aortic ECs, cytosolic Ca 2+ is captured by SERCA, released from the ER via RyRs, and extruded across the plasma membrane via the NCX. PMCA acts in parallel to this pathway to bind to and deliver Ca 2+ to the extracellular space; (2) Vectorial Ca 2+ release from sub-plasmalemmal InsP3Rs to the extracellular space via NCX [389] : this system operates following either a moderate or a slow increase in InsP3 levels in porcine coronary artery ECs, prevents subplasmalemmal Ca 2+ from reaching the deeper cytosol by triggering CICR on RyRs, and has, therefore, been termed SCCU.…”

Section: Microarchitecture Of the Ca 2+ Transporting Systems In Ecsmentioning

confidence: 99%

“…The microstructural physical localization of Ca 2+ pumps, transporters and channels in the ER and plasma membrane relative to each other determines the pattern of Ca 2+ clearance from the endothelial cytosol [36,40,41,138,139,345,388] . This organization of the Ca 2+ transporting systems creates Ca 2+ gradients between the sub-plasmalemmal region and bulk cytoplasm, which, in turn, enables the same second messenger, i.e., Ca 2+ , to regulate diverse cellular functions depending on its proximity to specific Ca 2+ -sensitive effectors [10] .…”

Section: Microarchitecture Of the Ca 2+ Transporting Systems In Ecsmentioning

confidence: 99%

“…A variety of pumps and exchangers fulfil the function to remove Ca 2+ from the cytosol following EC stimulation, namely SERCA, NCX, PMCA, and the mitochondrial uniporter [36,40,41,139,[343][344][345][346][347][348][349] . SERCA, NCX, PMCA, mitochondria may be aligned either in series or in parallel in ECs in order to remove Ca 2+ from the cytosol properly, to achieve successful ER Ca 2+ refilling, and facilitate SOCE by buffering sub-plasmalemmal Ca…”

Section: + Extrusion From the Cytosolmentioning

confidence: 99%

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Update on vascular endothelial Ca²⁺signalling: A tale of ion channels, pumps and transporters

Moccia

Berra‐Romani²,

Tanzi³

2012

WJBC

110

192

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A monolayer of endothelial cells (ECs) lines the lumen of blood vessels and forms a multifunctional transducing organ that mediates a plethora of cardiovascular processes. The activation of ECs from as state of quiescence is, therefore, regarded among the early events leading to the onset and progression of potentially lethal diseases, such as hypertension, myocardial infarction, brain stroke, and tumor. Intracellular Ca 2+ signals have long been know to play a central role in the complex network of signaling pathways regulating the endothelial functions. Notably, recent work has outlined how any change in the pattern of expression of endothelial channels, transporters and pumps involved in the modulation of intracellular Ca 2+ levels may dramatically affect whole body homeostasis. Vascular ECs may react to both mechanical and chemical stimuli by generating a variety of intracellular Ca 2+ signals, ranging from brief, localized Ca 2+ pulses to prolonged Ca 2+ oscillations engulfing the whole cytoplasm. The well-defined spatiotemporal profile of the subcellular Ca 2+ signals elicited in ECs by specific extracellular inputs depends on the interaction between Ca 2+ releasing channels, which are located both on the plasma membrane and in a number of intracellular organelles, and Ca 2+ removing systems. The present article aims to summarize both the past and recent literature in the field to provide a clear-cut picture of our current knowledge on the molecular nature and the role played by the components of the Ca 2+ machinery in vascular ECs under both physiological and pathological conditions.

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Bradykinin and histamine‐induced cytosolic calcium increase in capillary endothelial cells of bovine adrenal medulla

Vinet

Cortés

Álvarez

et al. 2014

Cell Biology International

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We have assessed the effect of bradykinin and histamine on the cytosolic free calcium concentration ([Ca(2+)]i ) of bovine adrenal medulla capillary endothelial cells (BAMCECs). To measure [Ca(2+)]i changes in BAMCECs the intracellular fluorescent probe, fluo-3 AM, was used. Bradykinin (3 µM) produced a transient monophasic increase in [Ca(2+)]i , which was depressed by B1650 (0.1 µM), a B2-bradykinin receptor antagonist (D-Arg-[Hyp(3), Thi(5,8) , D-Phe(7)]-Bradykinin). Similarly, increase in [Ca(2+)]i induced by histamine was also depressed by tripolidine (0.1 µM), an H1-histamine receptor antagonist. [Ca(2+)]i increase induced by both agonists was unaffected in the absence of extracellular Ca(2+) or presence of antagonists of voltage operated Ca(2+) channels (VOCCs). Thapsigargin (1 µM) did not abolish the increase of [Ca(2+)]i produced by bradykinin, but abolished that of histamine. In contrast, caffeine (100 µM), abolished the [Ca(2+)]i response induced by bradykinin (3 µM), but did not affect the [Ca(2+)]i increase induced by histamine (100 µM). The results indicate the presence of B2 bradykinin- and H1 histamine-receptors in BAMCECs. Liberation of Ca(2+) induced by both agonists occurs through 2 different intracellular mechanisms. While bradykinin activates a sarco(endo) plasmic reticulum (SER) containing a SER Ca(2+) -ATPase (SERCA) thapsigargin-insensitive, histamine activates a SER containing a SERCA thapsigargin-sensitive. We suggest that the increase in [Ca(2+)]i induced by bradykinin and histamine could be of physiological relevance, modulating adrenal gland microcirculation.

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Vectorial Ca2+ release via ryanodine receptors contributes to Ca2+ extrusion from freshly isolated rabbit aortic endothelial cells

Cited by 24 publications

References 26 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

Update on vascular endothelial Ca²⁺signalling: A tale of ion channels, pumps and transporters

Bradykinin and histamine‐induced cytosolic calcium increase in capillary endothelial cells of bovine adrenal medulla

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Vectorial Ca2+ release via ryanodine receptors contributes to Ca2+ extrusion from freshly isolated rabbit aortic endothelial cells

Cited by 24 publications

References 26 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

Update on vascular endothelial Ca2+signalling: A tale of ion channels, pumps and transporters

Bradykinin and histamine‐induced cytosolic calcium increase in capillary endothelial cells of bovine adrenal medulla

Contact Info

Product

Resources

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Update on vascular endothelial Ca²⁺signalling: A tale of ion channels, pumps and transporters