Аннотация:Mitochondria are large-scale regulators of cytosolic calcium (Ca2+)
under normal cellular conditions. In this paper we model the complex behavior
of mitochondrial calcium during the stimulation of a single cell by
increase of agonist generated inositol 1,4,5-trisphosphate (IP3) concentration
and find results that are in good agreement with recent experimental
studies. We also study the influence of the cellular network connectivity
on intercellular calcium signaling via gap junction diffusion of second
messengers. We include in our model the dependence of the junctional
conductivity on the cytosolic calcium concentrations in adjacent cells. We
consider three different mechanisms of calcium wave propagation through
gap junctions: via Ca2+ diffusion, IP3 diffusion, and both Ca2+ and IP3
diffusion. Our results suggest that IP3 diffusion is the mechanism of Ca2+
wave propagation and that Ca2+ diffusion is the mechanism of synchronization
of cytosolic Ca2+ oscillations in adjacent cells. We also study
the role of different topological configurations of cellular connectivity on
these phenomena. We argue that the most important issue in modelling
the intercellular calcium signaling is to account for the cellular topology of
the tissue. Our results suggest that the dynamics of the tissue is defined
by the topology of the connection graph of cells with each other.
Key words:Calcium wave, calcium signaling, inositol 1,4,5-trisphosphate,
mitochondrion, gap junction, network, connectivity, topology.