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Cytosolic calcium machinery is one of the principal signaling mechanisms
by which endothelial cells (ECs) respond to external stimuli during several biological
processes, including vascular progression in both physiological and pathological
conditions. Low concentrations of angiogenic factors (such as VEGF) activate in
fact complex pathways involving, among others, second messengers arachidonic acid
(AA) and nitric oxide (NO), which in turn control the activity of plasma membrane
calcium channels. The subsequent increase in the intracellular level of the ion regulates
fundamental biophysical properties of ECs (such as elasticity, intrinsic motility,
and chemical strength), enhancing their migratory capacity. Previously, a number
of continuous models have represented cytosolic calcium dynamics, while EC migration
in angiogenesis has been separately approached with discrete, lattice-based
techniques. These two components are here integrated and interfaced to provide a
multiscale and hybrid Cellular Potts Model (CPM), where the phenomenology of a
motile EC is realistically mediated by its calcium-dependent subcellular events. The
model, based on a realistic 3-D cell morphology with a nuclear and a cytosolic region,
is set with known biochemical and electrophysiological data. In particular, the resulting
simulations are able to reproduce and describe the polarization process, typical of
stimulated vascular cells, in various experimental conditions.Moreover, by analyzing
the mutual interactions between multilevel biochemical and biomechanical aspects,
our study investigates ways to inhibit cell migration: such strategies have in fact the
potential to result in pharmacological interventions useful to disrupt malignant vascular
progression
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