![]() Cell proliferation within small intestinal crypts is the principal driving force for cell migration on villi. This methodology can be applied to interrogate intestinal epithelial dynamics and characterize situations in which processes involved in cell turnover become uncoupled, including pharmacological treatments and disease models.—Parker, A., Maclaren, O. We conclude that cell proliferation within the crypt is the primary force that drives cell migration along the villus. Furthermore, halting and resuming proliferation results in the synchronized response of cell migration on the villi. We found that epithelial cell migration velocities along the villi are coupled to cell proliferation rates within the crypts in all conditions. We used established cell-tracking methods based on thymine analog cell labeling and developed tailored mathematical models to quantify cell proliferation and migration under normal conditions and when proliferation is reduced and when it is temporarily halted. Some reports suggest that proliferation and migration may not be related while other studies support a direct relationship. Nor is it known precisely how villus cell migration is affected when proliferation is perturbed. It is not known whether cell proliferation is sufficient to drive epithelial cell migration during homoeostatic turnover of the epithelium. The functional integrity of the intestinal epithelial barrier relies on tight coordination of cell proliferation and migration, with failure to regulate these processes resulting in disease. mutant PIK3CA) resulted in profoundly increased migration where extracellular multiscale directed migration cues and intrinsic signaling synergistically conspire to greatly outperform normal cells or any extracellular guidance cues in isolation.Ĭell proliferation within small intestinal crypts is the principal driving force for cell migration on villi However, while nanoscale cues promoted migration in all cases, microscale directed migration cues are dominant as the geometric constraint narrows, a behavior that is well explained by stochastic diffusion anisotropy modeling. We demonstrate that collective cell migration is profoundly enhanced by the addition of contract guidance cues when not otherwise constrained. This permits us to elucidate the influence, and parse out the relative contribution, of multiscale features, and define how these physical inputs are jointly processed with oncogenic signaling. To investigate complex biophysical relationships driving directed cell migration, we developed a biomimetic platform that allows perturbation of microscale geometric constraints with concomitant nanoscale contact guidance architectures. Multiscale Cues Drive Collective Cell Migration
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