Wheat germ agglutinin inhibits thrombin-induced rises in cytosolic free calcium and prostacyclin synthesis by human umbilical vein endothelial cells

1988 ◽  
Vol 137 (3) ◽  
pp. 553-558 ◽  
Author(s):  
J�rgen Grulich-Henn ◽  
Babette B. Weksler ◽  
Kentaro Watanabe ◽  
Eric A. Jaffe
Keyword(s):  
Endothelial Cells ◽  
Wheat Germ Agglutinin ◽  
Wheat Germ ◽  
Umbilical Vein ◽  
Free Calcium ◽  
Cytosolic Free Calcium ◽  
Human Umbilical Vein ◽  
Umbilical Vein Endothelial Cells ◽  
Prostacyclin Synthesis

scholarly journals Mechanisms involved in the stimulation of prostacyclin synthesis by human lymphocytes in human umbilical vein endothelial cells

2003 ◽  
Vol 139 (2) ◽  
pp. 321-328 ◽  
Author(s):  
Faten Merhi-Soussi ◽  
Zury Dominguez ◽  
Olga Macovschi ◽  
Madeleine Dubois ◽  
Georges Nemoz ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Umbilical Vein ◽  
Human Lymphocytes ◽  
Human Umbilical Vein ◽  
Umbilical Vein Endothelial Cells ◽  
Prostacyclin Synthesis ◽  
Stimulation Of

scholarly journals Evidence that agonists stimulate bivalent-cation influx into human endothelial cells

1988 ◽  
Vol 255 (1) ◽  
pp. 179-184 ◽  
Author(s):  
T J Hallam ◽  
R Jacob ◽  
J E Merritt
Keyword(s):  
Endothelial Cells ◽  
Plasma Membrane ◽  
Umbilical Vein ◽  
Free Calcium ◽  
Human Endothelial Cells ◽  
Bivalent Cation ◽  
Human Umbilical Vein ◽  
Fura 2 ◽  
Bivalent Cations ◽  
Umbilical Vein Endothelial Cells

Human umbilical-vein endothelial cells stimulated with thrombin or histamine show an increase in [Ca2+]i (cytoplasmic free calcium concn.) that is maintained well above the basal pre-stimulated value as long as agonist and a source of extracellular Ca2+ are present. These results provide circumstantial evidence that agonists stimulate influx of Ca2+ across the plasma membrane and into the cytoplasm. Here, we have used Mn2+ as the extracellular bivalent cation which can bind to the fluorescent Ca2+ indicator fura-2 to quench its fluorescence completely. Human umbilical-vein endothelial cells were loaded with fura-2 and, in the presence of extracellular Mn2+, thrombin and histamine were shown to cause quenching of the intracellular dye. This result demonstrates conclusively that agonists can stimulate the influx of bivalent cations. Stimulated discharge of Ca2+ from intracellular stores and influx of Mn2+ were temporally resolved in the same cells to show that release of Ca2+ from intracellular stores clearly precedes influx. Influx of Mn2+ was also demonstrated when extracellular Mn2+ was added after agonist at a time when [Ca2+]i had fallen back to the basal value, showing that influx is not dependent on elevated [Ca2+]i.

A mathematical model of cytosolic calcium dynamics in human umbilical vein endothelial cells

1996 ◽  
Vol 270 (5) ◽  
pp. C1556-C1569 ◽  
Author(s):  
T. F. Wiesner ◽  
B. C. Berk ◽  
R. M. Nerem
Keyword(s):  
Mathematical Model ◽  
Endothelial Cells ◽  
Calcium Release ◽  
Umbilical Vein ◽  
Kinetic Equations ◽  
Cytosolic Calcium ◽  
Receptor Activation ◽  
Free Calcium ◽  
Human Umbilical Vein ◽  
Umbilical Vein Endothelial Cells

Important among the responses of endothelial cells are cytosolic free calcium transients. These transients are mediated by several factors, including blood-borne agonists, extracellular calcium, and fluid-imposed shear forces. The transients are characterized by a rapid rise followed by a plateau phase. A base mathematical model is presented that reasonably reproduces the measured calcium transient in cultured human umbilical vein endothelial cells responding to thrombin. Kinetic equations for receptor activation and calcium mobilization comprise the model. A graded response of intracellular free calcium to increasing concentrations of agonist is predicted. Also predicted is the elevation of the peak value and the plateau level by steady nonspecific leak of calcium across the plasma membrane. The influences of capacitative calcium entry, calcium-induced calcium release, and buffering by cytosolic proteins are investigated parametrically. The model predicts significant depletion of cellular calcium in response to agonist stimulation.

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