Cellular Dewetting: Opening of Macroapertures in Endothelial Cells

David Gonzalez-Rodriguez, Madhavi P. Maddugoda, Caroline Stefani, Sebastien Janel, Frank Lafont, Damien Cuvelier, Emmanuel Lemichez, and Françoise Brochard-Wyart

Phys. Rev. Lett. 108, 218105 – Published 25 May 2012

Abstract

Pathogenic bacteria can cross from blood vessels to host tissues by opening transendothelial cell macroapertures (TEMs). To induce TEM opening, bacteria intoxicate endothelial cells with proteins that disrupt the contractile cytoskeletal network. Cell membrane tension is no longer resisted by contractile fibers, leading to the opening of TEMs. Here we model the opening of TEMs as a new form of dewetting. While liquid dewetting is irreversible, we show that cellular dewetting is transient. Our model predicts the minimum radius for hole nucleation, the maximum TEM size, and the dynamics of TEM opening, in good agreement with experimental data. The physical model is then coupled with biological experimental data to reveal that the protein missing in metastasis (MIM) controls the line tension at the rim of the TEM and opposes its opening.

Received 22 October 2011

DOI:https://doi.org/10.1103/PhysRevLett.108.218105

Authors & Affiliations

David Gonzalez-Rodriguez^1,*, Madhavi P. Maddugoda², Caroline Stefani², Sebastien Janel³, Frank Lafont³, Damien Cuvelier¹, Emmanuel Lemichez², and Françoise Brochard-Wyart¹

¹Institut Curie, CNRS UMR 168 and Université Paris 6, 11 rue Pierre et Marie Curie, 75248 Paris Cedex 05, France
²INSERM, U1065, Université de Nice-Sophia-Antipolis, Centre Méditerranéen de Médecine Moléculaire, C3M, Nice, F-06204 Cedex 3, France
³Center for Infection and Immunity of Lille, CNRS UM8204, INSERM U1019, Institut Pasteur de Lille, Université Lille Nord de France, Lille-F59021, France