The cell membrane of platelets is coated in glycoproteins, which carry negative charges. This means both that they repel each other and also that they do not stick to the endothelium, because the endothelium itself has an inner glycoprotein coat of negatively charged particles. Tissue damage two important consequences first there are a number of substances released locally which are involved in clot formation, second it exposes collagen and other tissue which has positive charges Platelets attracted to the damage site stick together, and to the damaged tissue. They undergo a number of changes. In about a minute a small plug of platelets can form which will block a small hole or tear in a vessel.
Prostaglandins Aggregating platelets release arachidonic acid, which is a prostaglandin precursor.
Some of this arachidonic acid is converted into thromboxane A2, a prostaglandin, which attracts more platelets to the site of damage. Thromboxane A2 also causes platelets to release ADP, which acts as a platelet to platelet signal. ADP causes platelets to send out processes and expose receptors for fibrin on their surface. Thus they become sticky. A positive feedback system sets up.