Figure 2.

Platelet spreading. (A) Under resting conditions platelets normally are non-adherent. Upon exposure to an activating agonist, platelets change shape by reorganizing cytoskeletal elements, leading to the formation of filopodia, followed by lamellipodia and an increase in surface area. When platelets are exposed to immobilized ligands in experiments in vitro, this shape change is known as platelet spreading. Light microscopy images shows actin arrangement and morphology of phalloidin-treated platelets exposed to non-coated coverslips (left) or coverslips pre-coated with collagen (middle) or fibrin (right). Images were taken using an inverted bright-field fluorescence microscope. Scale bar = 20 μm. (B) Schematic of processes that can be imaged during platelet spreading in vitro include (1) Cytoskeletal protein rearrangement, such as formation of actin nodules, microtubule organization and generation of stress fibers; (2) super resolution microscopy (dSTORM, SIM) can capture GPVI clustering (purple dots) and alignment along collagen fibers (green lines); (3) microvesicle formation can be imaged using optical systems that provide resolution below 150 nm; discrete cytoskeletal rearrangement occurs alongside calpain-dependent processes, where calcium-sensitive proteases detach membrane proteins, allowing membrane blebbing required for microvesicle release from platelets and megakaryocytes.