Na+/Ca2+ exchangers and Orai channels jointly refill endoplasmic reticulum (ER) Ca2+ via ER nanojunctions in vascular endothelial cells

[1]  A. Tepikin,et al.  Endoplasmic reticulum–plasma membrane junctions: structure, function and dynamics , 2016, The Journal of physiology.

[2]  S. Hallström,et al.  Functional impairment of endothelial cells by the antimycotic amphotericin B. , 2016, Biochemical and biophysical research communications.

[3]  A. Evans,et al.  Cytoplasmic nanojunctions between lysosomes and sarcoplasmic reticulum are required for specific calcium signaling , 2014, bioRxiv.

[4]  Andras T. Deak,et al.  N-arachidonoyl glycine suppresses Na+/Ca2+ exchanger-mediated Ca2+ entry into endothelial cells and activates BKCa channels independently of GPCRs , 2013, British journal of pharmacology.

[5]  A. Evans,et al.  Pan‐junctional sarcoplasmic reticulum in vascular smooth muscle: nanospace Ca2+ transport for site‐ and function‐specific Ca2+ signalling , 2013, The Journal of physiology.

[6]  F. Moccia,et al.  Update on vascular endothelial Ca(2+) signalling: A tale of ion channels, pumps and transporters. , 2012, World journal of biological chemistry.

[7]  N. Fameli,et al.  The role of cytoplasmic nanospaces in smooth muscle cell Ca2+ signalling , 2012, Protoplasma.

[8]  M. Yaqoob,et al.  Ca2+ Influx through Reverse Mode Na+/Ca2+ Exchange Is Critical for Vascular Endothelial Growth Factor-mediated Extracellular Signal-regulated Kinase (ERK) 1/2 Activation and Angiogenic Functions of Human Endothelial Cells* , 2011, The Journal of Biological Chemistry.

[9]  M. Frieden,et al.  Thapsigargin activates Ca²+ entry both by store-dependent, STIM1/Orai1-mediated, and store-independent, TRPC3/PLC/PKC-mediated pathways in human endothelial cells. , 2011, Cell calcium.

[10]  K. Kuo,et al.  A model for the generation of localized transient [Na+] elevations in vascular smooth muscle. , 2009, Biochemical and biophysical research communications.

[11]  M. Blaustein,et al.  The Pump, the Exchanger, and Endogenous Ouabain: Signaling Mechanisms That Link Salt Retention to Hypertension , 2009, Hypertension.

[12]  D. Poburko,et al.  Ca2+ signaling in smooth muscle: TRPC6, NCX, and LNats in nanodomains , 2008, Channels.

[13]  K. Kuo,et al.  A quantitative model for linking Na+/Ca2+ exchanger to SERCA during refilling of the sarcoplasmic reticulum to sustain [Ca2+] oscillations in vascular smooth muscle. , 2006, Cell calcium.

[14]  D. Poburko,et al.  Transient Receptor Potential Channel 6–Mediated, Localized Cytosolic [Na+] Transients Drive Na+/Ca2+ Exchanger–Mediated Ca2+ Entry in Purinergically Stimulated Aorta Smooth Muscle Cells , 2007, Circulation research.

[15]  K. Strait,et al.  Calcium regulation of endothelin-1 synthesis in rat inner medullary collecting duct. , 2007, American journal of physiology. Renal physiology.

[16]  M. Szewczyk,et al.  Ca2+-pumps and Na+–Ca2+-exchangers in coronary artery endothelium versus smooth muscle , 2007, Journal of cellular and molecular medicine.

[17]  C. Mannella,et al.  Structural and functional features and significance of the physical linkage between ER and mitochondria , 2006, The Journal of cell biology.

[18]  M. Frieden,et al.  The Role of Mitochondria for Ca2+ Refilling of the Endoplasmic Reticulum* , 2005, Journal of Biological Chemistry.

[19]  C. van Breemen,et al.  Vectorial Ca2+ release via ryanodine receptors contributes to Ca2+ extrusion from freshly isolated rabbit aortic endothelial cells. , 2004, Cell calcium.

[20]  N. Gaudreault,et al.  Pressure-dependent myogenic constriction of cerebral arteries occurs independently of voltage-dependent activation. , 2002, American journal of physiology. Heart and circulatory physiology.

[21]  P. Li,et al.  Ca2+ removal mechanisms in freshly isolated rabbit aortic endothelial cells , 2002 .

[22]  D. Poburko,et al.  The mechanism of phenylephrine‐mediated [Ca2+]i oscillations underlying tonic contraction in the rabbit inferior vena cava , 2001, The Journal of physiology.

[23]  A. Pries,et al.  Expression of ryanodine receptor type 3 and TRP channels in endothelial cells: comparison of in situ and cultured human endothelial cells. , 2001, Cardiovascular research.

[24]  Hiroshi Watanabe,et al.  Calcium signalling in endothelial cells. , 2000, Cardiovascular research.

[25]  M. Blaustein,et al.  Ouabain augments Ca(2+) transients in arterial smooth muscle without raising cytosolic Na(+). , 2000, American journal of physiology. Heart and circulatory physiology.

[26]  M. Frieden,et al.  Histamine‐induced Ca2+ oscillations in a human endothelial cell line depend on transmembrane ion flux, ryanodine receptors and endoplasmic reticulum Ca2+‐ATPase , 2000, The Journal of physiology.

[27]  S. Kohlwein,et al.  Na+/Ca2+ Exchange Facilitates Ca2+-dependent Activation of Endothelial Nitric-oxide Synthase* , 1999, The Journal of Biological Chemistry.

[28]  F. Protasi,et al.  Shape, size, and distribution of Ca(2+) release units and couplons in skeletal and cardiac muscles. , 1999, Biophysical journal.

[29]  B. Nilius,et al.  Membrane potential as a modulator of the free intracellular Ca2+ concentration in agonist-activated endothelial cells. , 1999, General physiology and biophysics.

[30]  G. Paltauf,et al.  Stealth ryanodine‐sensitive Ca2+ release contributes to activity of capacitative Ca2+ entry and nitric oxide synthase in bovine endothelial cells , 1998, The Journal of physiology.

[31]  F. Dignat-George,et al.  Evidence that human endothelial cells express different isoforms of Na,K‐ATPase , 1998, Journal of hypertension.

[32]  M. Sturek,et al.  Submaximal stimulation of porcine endothelial cells causes focal Ca2+ elevation beneath the cell membrane , 1998, The Journal of physiology.

[33]  B. Quednau,et al.  Tissue specificity and alternative splicing of the Na+/Ca2+ exchanger isoforms NCX1, NCX2, and NCX3 in rat. , 1997, The American journal of physiology.

[34]  M. Blaustein,et al.  Na+ pump low and high ouabain affinity alpha subunit isoforms are differently distributed in cells. , 1997, Proceedings of the National Academy of Sciences of the United States of America.

[35]  M. Dunn,et al.  Roles of calcium and kinases in regulation of thrombin-stimulated preproendothelin-1 transcription. , 1996, The American journal of physiology.

[36]  T. Iwamoto,et al.  A Novel Isothiourea Derivative Selectively Inhibits the Reverse Mode of Na+/Ca2+ Exchange in Cells Expressing NCX1* , 1996, The Journal of Biological Chemistry.

[37]  L. Vaca,et al.  Modulation of cell membrane potential in cultured vascular endothelium. , 1996, The American journal of physiology.

[38]  F. Curry,et al.  Measurement of membrane potential of endothelial cells in single perfused microvessels. , 1995, Microvascular research.

[39]  D. Grant,et al.  Electrophysiological characteristics of cultured human umbilical vein endothelial cells. , 1994, Microvascular research.

[40]  O. A. Cabello,et al.  Vectorial Ca2+ flux from the extracellular space to the endoplasmic reticulum via a restricted cytoplasmic compartment regulates inositol 1,4,5-trisphosphate-stimulated Ca2+ release from internal stores in vascular endothelial cells. , 1993, The Biochemical journal.

[41]  A. Marks,et al.  Anti-ryanodine receptor antibody binding sites in vascular and endocardial endothelium. , 1993, Circulation research.

[42]  David John Adams,et al.  Membrane potential and Na(+)-K+ pump activity modulate resting and bradykinin-stimulated changes in cytosolic free calcium in cultured endothelial cells from bovine atria. , 1990, The Journal of biological chemistry.

[43]  A. Bakhramov,et al.  Histamine‐induced inward currents in cultured endothelial cells from human umbilical vein , 1988, British journal of pharmacology.

[44]  L. Ignarro,et al.  Endothelium-derived relaxing factor produced and released from artery and vein is nitric oxide. , 1987, Proceedings of the National Academy of Sciences of the United States of America.

[45]  S. Moncada,et al.  Nitric oxide release accounts for the biological activity of endothelium-derived relaxing factor , 1987, Nature.

[46]  H. Ijichi,et al.  Effect of inhibition of Na+-K+ ATPase on the prostacyclin generation of cultured human vascular endothelial cells. , 1987, Life sciences.

[47]  S. Rapoport,et al.  Cerebrovascular Permeability Coefficients to Sodium, Potassium, and Chloride , 1986, Journal of neurochemistry.

[48]  R Y Tsien,et al.  Measurement of cytosolic free Ca2+ in individual small cells using fluorescence microscopy with dual excitation wavelengths. , 1985, Cell calcium.

[49]  C. Edgell,et al.  Permanent cell line expressing human factor VIII-related antigen established by hybridization. , 1983, Proceedings of the National Academy of Sciences of the United States of America.

[50]  A. Somlyo,et al.  SARCOPLASMIC RETICULUM AND EXCITATION-CONTRACTION COUPLING IN MAMMALIAN SMOOTH MUSCLES , 1972, The Journal of cell biology.

[51]  M. Frieden,et al.  Ca2+ refilling of the endoplasmic reticulum is largely preserved albeit reduced Ca2+ entry in endothelial cells. , 2007, Cell calcium.

[52]  K. Kuo,et al.  Calyculin-A disrupts subplasmalemmal junction and recurring Ca2+ waves in vascular smooth muscle. , 2005, Cell calcium.

[53]  D. Poburko,et al.  Organellar junctions promote targeted Ca2+ signaling in smooth muscle: why two membranes are better than one. , 2004, Trends in pharmacological sciences.

[54]  C. van Breemen,et al.  Ca(2+) removal mechanisms in freshly isolated rabbit aortic endothelial cells. , 2002, Cell calcium.

[55]  S. Kohlwein,et al.  Na(+)/Ca(2+) exchange facilitates Ca(2+)-dependent activation of endothelial nitric-oxide synthase. , 1999, The Journal of biological chemistry.

[56]  H. Strauss,et al.  Intracellular calcium, currents, and stimulus-response coupling in endothelial cells. , 1993, Hypertension.

[57]  C. van Breemen.  Calcium requirement for activation of intact aortic smooth muscle , 1977, The Journal of physiology.