Dynamics of Wound Closure in Living Nematic Epithelia

TL;DR

This paper models the wound closure process in living epithelial tissues as a 2D active nematic fluid, revealing how active stresses influence closure speed and defect dynamics, supported by experimental observations.

Contribution

It introduces a theoretical model of epithelial wound healing using active nematic fluid dynamics, linking active stresses and nematic order to wound closure behavior.

Findings

Contractile stresses accelerate wound closure.

Extensile stresses slow down closure.

Topological defects form and annihilate during healing.

Abstract

We study theoretically the closure of a wound in a layer of epithelial cells in a living tissue after damage. Our analysis is informed by our recent experiments observing re-epithelialisation in vivo of Drosophila pupae. On time and length-scales such that the evolution of the epithelial tissue near the wound is well captured by that of a 2D active fluid with local nematic order, we consider the free-surface problem of a hole in a bounded region of tissue, and study the role that active stresses far from the hole play in the closure of the hole. For parallel anchored nematic order at the wound boundary (as we observe in our experiments), we find that closure is accelerated when the active stresses are contractile and slowed down when the stresses are extensile. Parallel anchoring also leads to the appearance of topological defects which annihilate upon wound closure.