In primary airway epithelial cells, the unjamming transition is distinct from the epithelial-to-mesenchymal transition

Jennifer A. Mitchel, Amit Das, Michael J. O’Sullivan, Ian T. Stancil, Stephen J. DeCamp, Stephan Koehler, Oscar H. Ocaña, James P. Butler, Jeffrey J. Fredberg, M. Angela Nieto, Dapeng Bi and Jin-Ah Park ()
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Jennifer A. Mitchel: Harvard T.H. Chan School of Public Health
Amit Das: Northeastern University
Michael J. O’Sullivan: Harvard T.H. Chan School of Public Health
Ian T. Stancil: Harvard T.H. Chan School of Public Health
Stephen J. DeCamp: Harvard T.H. Chan School of Public Health
Stephan Koehler: Harvard T.H. Chan School of Public Health
Oscar H. Ocaña: Instituto de Neurociencias (CSIC-UMH)
James P. Butler: Harvard T.H. Chan School of Public Health
Jeffrey J. Fredberg: Harvard T.H. Chan School of Public Health
M. Angela Nieto: Instituto de Neurociencias (CSIC-UMH)
Dapeng Bi: Northeastern University
Jin-Ah Park: Harvard T.H. Chan School of Public Health

Nature Communications, 2020, vol. 11, issue 1, 1-14

Abstract: Abstract The epithelial-to-mesenchymal transition (EMT) and the unjamming transition (UJT) each comprises a gateway to cellular migration, plasticity and remodeling, but the extent to which these core programs are distinct, overlapping, or identical has remained undefined. Here, we triggered partial EMT (pEMT) or UJT in differentiated primary human bronchial epithelial cells. After triggering UJT, cell-cell junctions, apico-basal polarity, and barrier function remain intact, cells elongate and align into cooperative migratory packs, and mesenchymal markers of EMT remain unapparent. After triggering pEMT these and other metrics of UJT versus pEMT diverge. A computational model attributes effects of pEMT mainly to diminished junctional tension but attributes those of UJT mainly to augmented cellular propulsion. Through the actions of UJT and pEMT working independently, sequentially, or interactively, those tissues that are subject to development, injury, or disease become endowed with rich mechanisms for cellular migration, plasticity, self-repair, and regeneration.

Date: 2020
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DOI: 10.1038/s41467-020-18841-7

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