🩹 Wound Healing Cell Migration Simulator

About this simulation

When an epithelial sheet is wounded — in a lab "scratch assay" or in real skin — the cells bordering the gap do not simply crawl away one by one. They move as a coordinated sheet, extending actin-rich lamellipodia and pulling their neighbours along through cadherin cell-cell junctions, gradually closing the gap from both edges toward the centre.

How it works

• Growth factor concentration — chemokines and growth factors (e.g. EGF, FGF) released at the wound margin raise cell motility and set the baseline migration speed of the front.
• Cell-cell adhesion — this simulation follows the well-documented biphasic relationship: too little adhesion and cells detach and migrate individually (slow, disorganised); too much adhesion and the sheet jams and cannot deform. Migration is fastest at intermediate adhesion.
• Leader cells — the brighter, elongated cells at the front are "leader" cells that pull the follower sheet behind them, occasionally breaking ahead to form finger-like protrusions when adhesion is low.
• The pink strip visible in the gap is the exposed extracellular matrix (the "wound bed") which shrinks as new tissue covers it.

Controls

• Growth factor — baseline chemical stimulus driving migration speed.
• Cell-cell adhesion — coordination between neighbouring cells; peaks around the middle for fastest, most uniform closure.
• Wound gap width — how wide the initial injury is (rebuilds the tissue).
• Show chemokine gradient — toggles the diffusing growth-factor cloud overlay above the wound.
• ↺ Reset wound — restarts closure from a fresh gap. Drag to rotate, scroll to zoom.

Did you know?

Scratch assays remain one of the simplest and most widely used lab techniques for studying collective cell migration, and the same leader-follower dynamics shown here drive real processes like skin re-epithelialisation and, when dysregulated, cancer cell invasion.