Cellular dewetting: opening of macroapertures in endothelial cells.

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.

• Authors: David Gonzalez-Rodriguez, Madhavi P Maddugoda, Caroline Stefani, Sebastien Janel, Frank Lafont, Damien Cuvelier, Emmanuel Lemichez, Françoise Brochard-Wyart
• Journal: Physical review letters (Phys Rev Lett) Vol. 108 Issue 21 Pg. 218105 (May 25 2012) ISSN: 1079-7114 [Electronic] United States
• PMID: 23003307 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Bacterial Proteins
• Recombinant Proteins
• epidermal cell differentiation inhibitor, Staphylococcus aureus

Topics

• Bacterial Proteins (pharmacology)
• Cell Membrane (chemistry, drug effects, metabolism, ultrastructure)
• Human Umbilical Vein Endothelial Cells (chemistry, metabolism, microbiology, ultrastructure)
• Humans
• Microscopy, Fluorescence (methods)
• Models, Biological
• Recombinant Proteins (pharmacology)
• Wettability