Figure 1.

Adhesion system of platelets (platelet spreading and integrin activation). In resting platelets, αIIbβ3 integrins are in a bent and inactive conformation. Integrin activation can be triggered in 2 ways: (1) inside-out signaling or (2) outside-in signaling. In the first case integrin activation is initiated by platelet agonists such as thrombin. Thrombin activates the protease-activated GPCRs (G protein-coupled receptors), which leads to an increase in concentration of the cytosolic Ca²⁺. This triggers an intracellular signaling cascade that promotes talin binding to the cytoplasmic tail of the β2 chain. This event elicits integrin extension and activation. In the outside-in signaling, αIIbβ3 is activated by ligand binding (e.g., fibrinogen).