Cell based modeling of arteriosclerosis

Abstract

Thesis (B.S.)--University of Rochester. Dept. of Physics and Astronomy, 2005.Studying how mesenchymal cells organize to cause arteriosclerosis, a disease where the mesenchymal cells on the vascular wall of the arteries or on the cardiac valves turn to bone tissue and harden, could give insight into its cellular mechanisms. Mesenchymal cells secrete the morphogen activator bone morphogenic protein (BMP-2) and the inhibitor matrix carboxyglutamaic acid protein (MGP) that drive the formation of striped patterns. Previous continuum models (Garfinkel et al.) [3] can predict this pattern formation by displaying high concentrations of BMP-2. This model uses the reaction-diffusion equations to adjust the concentrations of the morphogens over time by having them fuel their own production autocatalytically. However, the Garfinkel et al. model omits the cells and assumes cellular signals even in the absence of cells, thus neglecting the cells' feedback. In order to make the model closer to how a biological system actually works a cell based model is needed. Our cellular Potts model substitutes autocatalytic production of BMP-2 for chemotactic recruitment of mesenchymal cells