A mathematical model of cytosolic calcium dynamics in human
umbilical vein endothelial cells.
Wiesner, Theodore F., Bradford C. Berk, Robert M. Nerem.
Bioengineering Center, Georgia Institute of Technology, Atlanta,
Ga. 30332-0405, Director of Cardiovascular Research, University of
Washington, Seattle, Washington 98195, Bioengineering Center, Georgia
Institute of Technology
APStracts 2:0422C, 1995.
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 which reasonably reproduces the measured Ca2+ 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 both the peak value and the
plateau level by steady non-specific 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.
Received 20 January 1995; accepted in final form 8 November 1995.
APS Manuscript Number C39-5.
Article publication pending Am. J. Physiol. (Cell Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 8 December 95