Cellular dewetting: opening of macroapertures in endothelial cells.

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.

Citation

David Gonzalez-Rodriguez, Madhavi P Maddugoda, Caroline Stefani, Sebastien Janel, Frank Lafont, Damien Cuvelier, Emmanuel Lemichez, Françoise Brochard-Wyart. Cellular dewetting: opening of macroapertures in endothelial cells. Physical review letters. 2012 May 25;108(21):218105

Mesh Tags

Substances

PMID: 23003307

search → result