Matrix Mechanics and Cell Contractility in Angiogenesis - Mechanical and Chemical Signaling in Angiogenesis - page 145

Fig. 2 Signaling diagram depicting the interplay of cell shape and cytoskeletal tension on EC
proliferation. Mediators of cell contractility (classical Rho-mediated elements) are shown in
green, mediators of cell-cycle progression are shown in blue, and cell-cycle decisions are
shown in red. Noco nocodazole; CytoD cytochalasin D; MT Org microtubule organization; CSK
cytoskeletal; Rb-P, phosphorylated-Rb. See text for citations
increases in actin stress fiber formation indicating that RhoA is required for contact-
mediated increases in proliferation [ 42 ]. Additionally, regions of EC proliferation
have been shown to be correlated with high traction stresses [ 43 ]. Inhibiting acto-
myosin tension or cadherin-mediated cell-cell interactions can alter the pattern of
proliferation. These data indicate that cell-cell interactions influence cytoskeletal
interactions that mediate EC proliferation.
3 Endothelial Cell Mechanosensing
In addition to mediating changes in cell spreading and growth, phenotypic changes
important for the progression of angiogenesis, the mechanical environment also
influences the mechanical properties of ECs. Sensitivity to the external mechanical
environment is made possible by cellular machinery that converts mechanical
signals into changes in cell stiffness [ 44 ] or gene expression [ 22 ].