Junctional and cytoplasmic contributions in wound healing.

Wound healing is characterized by the re-epitheliation of a tissue through the activation of contractile forces concentrated mainly at the wound edge. While the formation of an actin purse string has been identified as one of the main mechanisms, far less is known about the effects of the viscoelastic properties of the surrounding cells, and the different contribution of the junctional and cytoplasmic contractilities. In this paper, we simulate the wound healing process, resorting to a hybrid vertex model that includes cell boundary and cytoplasmic contractilities explicitly, together with a differentiated viscoelastic rheology based on an adaptive rest-length. From experimental measurements of the recoil and closure phases of wounds in the Drosophila wing disc epithelium, we fit tissue viscoelastic properties. We then analyse in terms of closure rate and energy requirements the contributions of junctional and cytoplasmic contractilities. Our results suggest that reduction of junctional stiffness rather than cytoplasmic stiffness has a more pronounced effect on shortening closure times, and that intercalation rate has a minor effect on the stored energy, but contributes significantly to shortening the healing duration, mostly in the later stages.