Speaker
Description
The corneal epithelium is a self-renewing tissue maintained with remarkable precision. Its regeneration is driven by limbal epithelial stem cells (LESCs), which reside at the corneal periphery and give rise to transit amplifying cells (TACs) that migrate centripetally toward the centre. These TACs continually replenish the tissue and, together with vertical delamination between layers, sustain the five to seven stratified layers of the epithelium. Despite this highly coordinated renewal process, the mechanical mechanisms regulating epithelial stratification remain poorly understood.
In this talk, I present simulation results demonstrating that stratification is strongly coupled to TAC proliferation, whereas LESC activity remains largely unchanged, consistent with their slow-cycling behaviour. Weakening cell–substrate adhesion increases epithelial turnover without the need for external growth factor stimulation. In addition, increased surface shedding promotes both cell division and delamination, while excessive shedding induces mechanical compensation in the form of cell stretching in the upper epithelial layer.
The model further predicts a direct relationship between the shedding rate and the centripetal velocity of clonal expansion, reflecting a wound-healing-like acceleration of epithelial migration. Overall, these results highlight how intercellular mechanical forces coordinate cell size, migration, and turnover to maintain and rapidly restore epithelial integrity. Finally, I introduce an extension of the model to a five-layer epithelial structure and demonstrate the resulting wound healing dynamics.
