| Summary: | At cell-matrix contacts, an elastocapillary effect arises in addition to active cell traction. The coexistence of active extracellular traction and other interfacial forces at the contacts blurs their distinctive roles in tissue morphogenesis, wound healing, and cancer metastasis. Here, we first observe that cell colonies can indent soft hydrogels, forming dimples. At inhibited cell contractility, the dimples still occur but with a reduced depth. To exclude active cell traction at the cell-matrix contact, we inhibit cell contractility and measure the interfacial stresses at the colony-hydrogel-medium three-phase interfaces using the Neumann triangle method. The critical elastocapillary length scale of the colony-hydrogel contacts is found to be comparable to the cell colony size, at which the classical Johnson-Kendall-Roberts contact theory fails. Theoretical and computational models suitable for different critical elastocapillary length scales are developed to predict the elastocapillarity-induced indentation depth. A two-step traction force microscopy is, therefore, proposed to separate active cell traction from the interfacial stresses. By quantifying the elastocapillary effect separated from active cell traction, our study lays down a foundation for understanding a variety of elastocapillarity-induced mechanobiological processes in cells and tissues.
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