# '''Platelet plug formation:''' [[Platelet]]s adhere to damaged endothelium to form a platelet plug (''primary hemostasis'') and then degranulate. This process is regulated through [[thromboregulation]]. Plug formation is activated by a [[glycoprotein]] called [[Vonvon Willebrand factor]] (vWF), which is found in [[Blood plasma|plasma]]. Platelets play one of major roles in the hemostatic process. When platelets come across the injured endothelium cells, they change shape, release granules and ultimately become ‘sticky’. Platelets express certain receptors, some of which are used for the adhesion of platelets to collagen. When platelets are activated, they express glycoprotein receptors that interact with other platelets, producing aggregation and adhesion. Platelets release cytoplasmic granules such as [[adenosine diphosphate]] (ADP), [[serotonin]] and [[thromboxane A2]]. Adenosine diphosphate (ADP) attracts more platelets to the affected area, serotonin is a vasoconstrictor and thromboxane A2 assists in platelet aggregation, vasoconstriction and degranulation. As more chemicals are released more platelets stick and release their chemicals; creating a platelet plug and continuing the process in a [[positive feedback]] loop. Platelets alone are responsible for stopping the bleeding of unnoticed wear and tear of our skin on a daily basis. This is referred to as primary hemostasis.<ref name=":0" /><ref>{{Cite journal|last=Li|first=Zhenyu|date=11 Nov 2010|title=Signaling during platelet adhesion and activation|journal=Arteriosclerosis, Thrombosis, and Vascular Biology|doi=10.1161/ATVBAHA.110.207522|pmid=21071698|volume=30|issue=12|pages=2341–2349|pmc=3085271}}</ref>