Biomedical Engineering Reference
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FIGURE 6.6: VEGF-induced chemotactic migration and cell polarization.
Representative three-dimensional views taken at 45 min intervals until t = 6
h. Red dot represents the VEGF source. (A) The cell, after a short latency,
rapidly polarizes establishing a leading edge, a long and thin pseudopodium,
which gives the direction of motion. (B) For comparison purposes, model re-
sults in the case of a monocompartmental endothelial cell (i.e., formed by
a unique unit representing an undifferentiated cytoplasm). All the other pa-
rameters are the same as in the previous case. It is worth to notice that this
approach is unable to reproduce cell polarization, as the cell is only a deformed
mass that moves toward the chemical source.
derlying cell movement. The relative literature in this field is vast and we
refer the reader to the comprehensive biochemical reviews [311, 323] and the
classical topics [7, 190]. In reality, the external chemical stimulus, via surface
receptors, triggers in fact the polymerization of the cell cytoskeleton, which
results in the constant abutting of the cell PM in the direction of motion and
in the coordinated development and release of focal adhesions (FAs). During
the motion of the overall cell, the nucleus is unable to have an autonomous
directional movement, as it only negligibility fluctuates in the cytoplasmic
fluid. However, the nucleus is anchored to intermediate actin filaments and
microtubules, which are in turn linked to the extracellular matrix through the
focal adhesion clusters: therefore, it is passively pulled by active forces trans-
mitted by the substrate via the cytoskeletal components (see the review [404]
and the references therein). Such indirect mechanical interactions between the
nucleus and the matrix environment are implicitly reproduced by the model
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