These agonists together with locally produced thrombin contribute to cellular activation by stimulating receptors that couple to heterotrimeric G proteins, which induce different signaling events and act synergistically to induce full platelet activation. This interaction allows the cells to establish contacts with collagen through the immunoglobulin-like GPVI, which triggers intracellular signals that lead to cellular activation and the release of the secondary mediators adenosine diphosphate (ADP) and thromboxane A 2 (TxA 2). Under conditions of high shear, the initial recruitment of platelets to the ‘reactive surface’ is mediated by the reversible interaction between the platelet receptor glycoprotein (GP)Ib and collagen-bound von Willebrand factor (vWF). Platelet adhesion and aggregation on the exposed extracellular matrix (ECM) requires the coordinated interaction of different platelet surface receptors with adhesive macromolecules.
0 Comments
Leave a Reply. |