dorsal/arxiv
View SchemaContact-inhibited chemotaxis in de novo and sprouting blood-vessel growth
| Authors | Roeland M. H. Merks, Erica D. Perryn, Abbas Shirinifard, James A. Glazier |
|---|---|
| Categories | |
| ArXiv ID | q-bio/0505033 |
| URL | https://arxiv.org/abs/q-bio/0505033 |
| DOI | 10.1371/journal.pcbi.1000163 |
| Journal | PLoS Computational Biology 2008, 4(9): e1000163 |
Abstract
Blood vessels form either when dispersed endothelial cells (the cells lining the inner walls of fully-formed blood vessels) organize into a vessel network (vasculogenesis), or by sprouting or splitting of existing blood vessels (angiogenesis). Although they are closely related biologically, no current model explains both phenomena with a single biophysical mechanism. Most computational models describe sprouting at the level of the blood vessel, ignoring how cell behavior drives branch splitting during sprouting. We present a cell-based, Glazier-Graner-Hogeweg-model simulation of the initial patterning before the vascular cords form lumens, based on plausible behaviors of endothelial cells. The endothelial cells secrete a chemoattractant, which attracts other endothelial cells. As in the classic Keller-Segel model, chemotaxis by itself causes cells to aggregate into isolated clusters. However, including experimentally-observed adhesion-driven contact inhibition of chemotaxis in the simulation causes randomly-distributed cells to organize into networks and cell aggregates to sprout, reproducing aspects of both de novo and sprouting blood-vessel growth. We discuss two branching instabilities responsible for our results. Cells at the surfaces of cell clusters attempting to migrate to the centers of the clusters produce a buckling instability. In a model variant that eliminates the surface-normal force, a dissipative mechanism drives sprouting, with the secreted chemical acting both as a chemoattractant and as an inhibitor of pseudopod extension. The branching instabilities responsible for our results, which result from contact inhibition of chemotaxis, are both generic developmental mechanisms and interesting examples of unusual patterning instabilities.
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"abstract": "Blood vessels form either when dispersed endothelial cells (the cells lining\nthe inner walls of fully-formed blood vessels) organize into a vessel network\n(vasculogenesis), or by sprouting or splitting of existing blood vessels\n(angiogenesis). Although they are closely related biologically, no current\nmodel explains both phenomena with a single biophysical mechanism. Most\ncomputational models describe sprouting at the level of the blood vessel,\nignoring how cell behavior drives branch splitting during sprouting. We present\na cell-based, Glazier-Graner-Hogeweg-model simulation of the initial patterning\nbefore the vascular cords form lumens, based on plausible behaviors of\nendothelial cells. The endothelial cells secrete a chemoattractant, which\nattracts other endothelial cells. As in the classic Keller-Segel model,\nchemotaxis by itself causes cells to aggregate into isolated clusters. However,\nincluding experimentally-observed adhesion-driven contact inhibition of\nchemotaxis in the simulation causes randomly-distributed cells to organize into\nnetworks and cell aggregates to sprout, reproducing aspects of both de novo and\nsprouting blood-vessel growth. We discuss two branching instabilities\nresponsible for our results. Cells at the surfaces of cell clusters attempting\nto migrate to the centers of the clusters produce a buckling instability. In a\nmodel variant that eliminates the surface-normal force, a dissipative mechanism\ndrives sprouting, with the secreted chemical acting both as a chemoattractant\nand as an inhibitor of pseudopod extension. The branching instabilities\nresponsible for our results, which result from contact inhibition of\nchemotaxis, are both generic developmental mechanisms and interesting examples\nof unusual patterning instabilities.",
"arxiv_id": "q-bio/0505033",
"authors": [
"Roeland M. H. Merks",
"Erica D. Perryn",
"Abbas Shirinifard",
"James A. Glazier"
],
"categories": [
"q-bio.TO",
"q-bio.CB"
],
"doi": "10.1371/journal.pcbi.1000163",
"journal_ref": "PLoS Computational Biology 2008, 4(9): e1000163",
"title": "Contact-inhibited chemotaxis in de novo and sprouting blood-vessel growth",
"url": "https://arxiv.org/abs/q-bio/0505033"
},
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