TY - JOUR
T1 - One-dimensional elastic continuum model of enterocyte layer migration
AU - Mi, Qi
AU - Swigon, David
AU - Rivière, Béatrice
AU - Cetin, Selma
AU - Vodovotz, Yoram
AU - Hackamz, David J.
N1 - Funding Information:
Q.M., B.R., and Y.V. acknowledge support from National Institutes of Health 2P50 GM053789-09. D.S. acknowledges support by Alfred P. Sloan Fellowship. B.R. also acknowledges support from National Science Foundation DMS 0506039. Y.V. also acknowledges support by grant from the Commonwealth of Pennsylvania. D.J.H. acknowledges support from National Institutes of Health R01 GM8238-01.
PY - 2007/12/1
Y1 - 2007/12/1
N2 - Necrotizing enterocolitis is the leading cause of death from gastrointestinal disease in preterm infants. It results from an injury to the mucosal lining of the intestine, leading to translocation of bacteria and endotoxin into the circulation. Intestinal mucosal defects are repaired by the process of intestinal restitution, during which enterocytes migrate from healthy areas to sites of injury. In this article, we develop a mathematical model of migration of enterocytes during experimental necrotizing enterocolitis. The model is based on a novel assumption of elastic deformation of the cell layer and incorporates the following effects: i), mobility promoting force due to lamellipod formation, ii), mobility impeding adhesion to the cell matrix, and iii), enterocyte proliferation. Our model successfully reproduces the behavior observed for enterocyte migration on glass coverslips, namely the dependence of migration speed on the distance from the wound edge, and the finite propagation distance in the absence of proliferation that results in an occasional failure to close the wound. It also qualitatively reproduces the dependence of migration speed on integrin concentration. The model is applicable to the closure of a wound with a linear edge and, after calibration with experimental data, could be used to predict the effect of chemical agents on mobility, adhesion, and proliferation of enterocytes.
AB - Necrotizing enterocolitis is the leading cause of death from gastrointestinal disease in preterm infants. It results from an injury to the mucosal lining of the intestine, leading to translocation of bacteria and endotoxin into the circulation. Intestinal mucosal defects are repaired by the process of intestinal restitution, during which enterocytes migrate from healthy areas to sites of injury. In this article, we develop a mathematical model of migration of enterocytes during experimental necrotizing enterocolitis. The model is based on a novel assumption of elastic deformation of the cell layer and incorporates the following effects: i), mobility promoting force due to lamellipod formation, ii), mobility impeding adhesion to the cell matrix, and iii), enterocyte proliferation. Our model successfully reproduces the behavior observed for enterocyte migration on glass coverslips, namely the dependence of migration speed on the distance from the wound edge, and the finite propagation distance in the absence of proliferation that results in an occasional failure to close the wound. It also qualitatively reproduces the dependence of migration speed on integrin concentration. The model is applicable to the closure of a wound with a linear edge and, after calibration with experimental data, could be used to predict the effect of chemical agents on mobility, adhesion, and proliferation of enterocytes.
UR - http://www.scopus.com/inward/record.url?scp=36849055522&partnerID=8YFLogxK
U2 - 10.1529/biophysj.107.112326
DO - 10.1529/biophysj.107.112326
M3 - Article
C2 - 17704181
AN - SCOPUS:36849055522
SN - 0006-3495
VL - 93
SP - 3745
EP - 3752
JO - Biophysical Journal
JF - Biophysical Journal
IS - 11
ER -