Abstract
Cellular adhesions have the remarkable property that they adapt their stability to the applied mechanical load. Here, authors describe a generic physical mechanism that explains self-stabilization of idealized adhesion systems under shear. Mechanical loading generally weakens adhesive structures and eventually leads to their rupture. However, biological systems can adapt to loads by strengthening adhesions, which is essential for maintaining the integrity of tissue and whole organisms. Inspired by cellular focal adhesions, we suggest here a generic, molecular mechanism that allows adhesion systems to harness applied loads for self-stabilization through adhesion growth. The mechanism is based on conformation changes of adhesion molecules that are dynamically exchanged with a reservoir. Tangential loading drives the occupation of some states out of equilibrium, which, for thermodynamic reasons, leads to association of further molecules with the cluster. Self-stabilization robustly increases adhesion lifetimes in broad parameter ranges. Unlike for catch-bonds, bond rupture rates can increase monotonically with force. The self-stabilization principle can be realized in many ways in complex adhesion-state networks;we show how it naturally occurs in cellular adhesions involving the adaptor proteins talin and vinculin.
Dokumententyp: | Zeitschriftenartikel |
---|---|
Fakultät: | Tiermedizin |
Themengebiete: | 600 Technik, Medizin, angewandte Wissenschaften > 610 Medizin und Gesundheit |
Sprache: | Englisch |
Dokumenten ID: | 112600 |
Datum der Veröffentlichung auf Open Access LMU: | 02. Apr. 2024, 07:38 |
Letzte Änderungen: | 02. Apr. 2024, 07:38 |