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Contact-inhibited chemotactic motility can drive both vasculogenesis and sprouting angiogenesis | | Roeland M. H. Merks
; James A. Glazier
; | | Date: |
17 May 2005 | | Subject: | Tissues and Organs; Cell Behavior | q-bio.TO q-bio.CB | | Abstract: | Blood vessels can develop either through vasculogenesis, in which endothelial cells--the cells lining the inner walls of arteries and veins--aggregate and form a vascular network, or through angiogenesis: sprouting or splitting of existing blood vessels. Many computational models exist to explain and describe either vasculogenesis or angiogenesis. However, since the same genetic machinery drives both, a plausible mechanism should explain both. Here we present a cell-centered, hybrid Cellular-Potts/Partial Differential Equation Model that reproduces aspects of both sprouting angiogenesis and vasculogenesis. The model assumes that endothelial cells autocrinically secrete a chemoattractant which decays in the extracellular matrix. Vascular network formation requires an additional biologically realistic contact-inhibition mechanism, that represses chemotactic filopodia at cell-cell interfaces (e.g. mediated by vascular-endothelial-cadherin). This mechanism also drives a sprouting instability, transforming round cell clusters into vascular networks, a process resembling angiogenesis. | | Source: | arXiv, q-bio.TO/0505033 | | Services: | Forum | Review | PDF | Favorites | |
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