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Researchers developed a mathematical framework to analyze how cell monolayers close large circular wounds, separating the contributions of cell growth, elastic tissue deformation, and fluid-like cell rearrangement. Applied to mouse embryonic epicardial cells, the model revealed that wound closure requires both tissue fluidity and elastic fiber reinforcement, with cells treated with TGF-β showing reduced fluidity and increased elastic deformation compared to untreated cells. The framework enables quantitative measurement of these distinct mechanical processes from experimental observations of tissue movement.
Why it matters
This work provides a tool for understanding tissue repair mechanisms at a quantitative level, which could inform strategies for improving wound healing in medical contexts. The ability to separately measure growth, elastic, and fluid contributions to tissue closure may help identify therapeutic targets for conditions where wound healing is impaired or excessive.
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⚠️ Preprint – Noch nicht peer-reviewed
Dieser Artikel wurde noch nicht von unabhängigen Experten begutachtet. Die Ergebnisse sind vorläufig und sollten mit Vorsicht interpretiert werden.
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Abstract: Large-scale circular gap closure occurs over a time scale on which cell growth and proliferation become important. Growth is the main driver of the closing process, while cell dynamics such as elongation and intercalation reflect elastic and fluidic contributions to tissue deformation. We develop a novel fluidized growth-elasticity framework as a nonlinear analogue of a Maxwell fluid with growth. The framework decomposes the experimentally observable strain rate into the additive sum of the growth, elastic, and fluidic strain rates, thus enabling the separate quantification of these contributions from tissue kinematics and allowing the roles of tissue elasticity and fluidity (the inverse of viscosity) to be characterized. We apply the model to large circular gaps ($sim$1.7 mm in diameter) in confluent monolayers of mouse embryonic epicardial cells (MEC1) under two conditions, without and with TGF-$beta$ treatment. We show that both tissue fluidity and the elastic properties associated with fiber reinforcement are critical for reproducing the closure kinematics. Specifically, we predict that the treated condition has lower fluidity, associated with a lower fluidic deformation rate and a higher elastic deformation rate than the untreated condition, in agreement with the experimental observations.