The paper's central contribution is a novel two-rod tensile testing device: monolayers are cultured on a sacrificial collagen scaffold between NiTi wires, released by collagenase digestion, and stretched while force is read from cantilever deflection calibrated against PDMS standards . This design satisfies four stated requirements β load borne only by the monolayer, minimal sample manipulation, live imaging during stretch, and quantitative force readout β a genuinely clever solution to the confounding that plagues substrate-attached measurements.
Tissue stiffness was E = 20 Β± 2 kPa (N = 12 controls), roughly 100-fold above transverse AFM measurements of constituent cells; monolayers tolerated 69 Β± 14% strain before failing, mostly by rod delamination. Nick experiments forced intercellular rupture, yielding adhesion energy Ξ β 0.07 N/m and a per-cell separation force of ~1.7 ΞΌN versus ~200 nN for doublets contacted only ~30 min β evidence that junctions mature toward far stronger coupling in confluent tissue . Perturbations cleanly parsed contributors: latrunculin B halved stiffness (10 Β± 6 kPa), Rho-kinase inhibition reduced it 36% (13 Β± 6 kPa), and EDTA cadherin disruption collapsed it to 0.8 Β± 0.4 kPa (N = 8β12 per group) .
Texture correlation showed tissue strain (Ξ΅xx = 50 Β± 6%) matched cellular strain measured from segmented E-cadherin-GFP images, with conserved cell volume and transverse thinning β no intercalation on ~5 min timescales. Myosin regulatory light chain relocalized to junctions upon substrate removal, and keratin filaments transitioned from wavy to taut under high strain, supporting a nonlinear load-bearing role consistent with prior keratin network work . High-stress creep showed power-law behavior (Ξ² = 0.15 Β± 0.03, below single-cell values of ~0.3β0.5) with a stress threshold separating solid-like from fluid-like response.
Assumptions for the simulated curve: linear region slope fixed at 20 kPa, toe extends to ~25% strain, plateau near failure, per reported qualitative features; values are illustrative, not measured.
Strengths include device calibration against independent PDMS measurements, live/dead and polarity controls confirming monolayer health for >3 h post-digestion, and strain-rate insensitivity confirming quasi-static loading. Key limitations: stress normalization assumes uniform ~10 ΞΌm monolayer thickness; failure is dominated by cellβrod adhesion, so doublet-force estimates require a fracture-mechanics model with assumed cell diameter (a β 10 ΞΌm); only MDCK-II is tested, so generality across epithelia is asserted, not shown; sample sizes are modest (N = 8β12); and the keratin mechanistic claim remains correlative β the authors themselves note it "will necessitate further study." The later literature the paper seeded β collective-migration and fluidization modeling and mechanochemical homeostasis work on the same MDCK system β confirms the paper's lasting influence. What would change the conclusions: intercalation-dominated extension at longer timescales, or keratin-disruption experiments showing no effect on high-strain stiffness.
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