Signaling during platelet adhesion and activation

Zhenyu Li, M. Keegan Delaney, Kelly A. O'Brien, Xiaoping Du

Research output: Contribution to journalArticlepeer-review

664 Scopus citations

Abstract

Upon vascular injury, platelets are activated by adhesion to adhesive proteins, such as von Willebrand factor and collagen, or by soluble platelet agonists, such as ADP, thrombin, and thromboxane A2. These adhesive proteins and soluble agonists induce signal transduction via their respective receptors. The various receptor-specific platelet activation signaling pathways converge into common signaling events that stimulate platelet shape change and granule secretion and ultimately induce the "inside-out" signaling process leading to activation of the ligand-binding function of integrin αIIbβ3. Ligand binding to integrin αIIbβ3 mediates platelet adhesion and aggregation and triggers "outside-in" signaling, resulting in platelet spreading, additional granule secretion, stabilization of platelet adhesion and aggregation, and clot retraction. It has become increasingly evident that agonist-induced platelet activation signals also cross talk with integrin outside-in signals to regulate platelet responses. Platelet activation involves a series of rapid positive feedback loops that greatly amplify initial activation signals and enable robust platelet recruitment and thrombus stabilization. Recent studies have provided novel insight into the molecular mechanisms of these processes.

Original languageEnglish
Pages (from-to)2341-2349
Number of pages9
JournalArteriosclerosis, Thrombosis, and Vascular Biology
Volume30
Issue number12
DOIs
StatePublished - Dec 2010

Keywords

  • G proteins
  • adhesion molecules
  • platelets
  • receptors
  • signal transduction

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

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