Final answer:
When cells like platelets encounter a vessel wall with specific ligands, they may adhere to it using transmembrane receptors, with this process being stabilized by von Willebrand factor. Actively generated internal stresses and motor proteins produce forces that contribute to adhesion.
Step-by-step explanation:
The process of a cell getting stuck on the vessel wall involves several biochemical and physical steps. Initially, animal cells in suspension typically exhibit a round shape due to the effective surface tension created by the plasma membrane and actin cortex.
For example, during the formation of a blood clot, platelets initially floating in the plasma bind to exposed collagen and endothelial lining at sites of vessel injury. This binding is stabilized by the glycoprotein known as von Willebrand factor. The platelets then release chemicals to contribute to hemostasis.
Additionally, adhesion is a dynamic process that can occur between moving surfaces. Here, actin retrograde flow influences the formation and maturation of adhesions between the cell and the substrate.
Furthermore, cells generate internal stresses involving motor proteins and ATP consumption, which lead to both normal and lateral contractile forces. These actively generated forces allow cells to probe the physical properties of their environment, contributing to cellular adhesion.
In the event of vessel obstruction, like a pulmonary embolism, cells such as red blood cells can become trapped in a clot preventing their escape. This is due to cellular and molecular adhesion events that may occur on the vessel walls.