Abstract
SummaryPreferential locations of atherosclerotic plaque are strongly associated with the areas of low wall shear stress and disturbed haemodynamic characteristics such as flow detachment, flow recirculation and oscillatory flow. The areas of low wall shear stress are also associated with the reduced production of adenosine triphosphate in the endothelial layer, as well as the resulting reduced production of inositol trisphosphate (IP3). The subsequent variation in Ca2+ signalling and nitric oxide synthesis could lead to the impairment of the atheroprotective function played by nitric oxide. In previous studies, it has been suggested that the reduced IP3 and Ca2+ signalling can explain the correlation of atherosclerosis with induced low WSS and disturbed flow characteristics. The massively parallel implementation described in this article provides insight into the dynamics of coupled smooth muscle cells and endothelial cells mapped onto the surface of an idealised arterial bifurcation. We show that variations in coupling parameters, which model normal and pathological conditions, provide vastly different smooth muscle cell Ca2+ dynamics and wave propagation profiles. The extensibility of the coupled cells model and scalability of the implementation provide a solid framework for in silico investigations of the interaction between complex cellular chemistry and the macro‐scale processes determined by fluid dynamics. © 2016 The Authors. International Journal for Numerical Methods in Biomedical Engineering published by John Wiley & Sons Ltd.
Highlights
The recently coined term in silico research refers to computer simulations of complex biological systems dynamics
This study investigates temporal and spatial cellular dynamics of large populations of coupled endothelial cells (ECs) and smooth muscle cells (SMCs) with the view of gaining insight into the Ca2C signalling in arterial wall tissue
We explore the relationship of calcium dynamics and arterial geometry as a way of determining how spatially and time-varying agonist concentration can produce calcium transients over much larger scales than a single cell, giving credence to the idea that plaques grow both upstream and downstream
Summary
The recently coined term in silico research refers to computer simulations of complex biological systems dynamics. The large-scale physiological simulations described here were designed to provide insight into the effects of the luminal concentration variations on adenosine triphosphate (ATP)-dependent dynamics in the coupled endothelial cells (ECs) and smooth muscle cells (SMCs) making up an arterial wall. The simulations of this nature provide a unique opportunity to perform experiments, which would never be possible in the in vivo and in vitro settings. Various specific pathological conditions, as described further in the text, can be simulated by changing the homocellular and heterocellular coupling parameters Numerical simulations of this nature have never been attempted before at the scale of millions of coupled cells
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