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Redox modification of platelet glycoproteins
1Department of Medicine, Division of Hematology, The University of Texas Health Science Center at San Antonio, San Antonio, Texas 78229, USA. essex@uthscsa.edu
Current Drug Targets
|November 1, 2006
Summary
Platelet glycoprotein receptors, like alphaIIb betaIIIa, have redox-sensitive thiols crucial for aggregation. Modulating this platelet redox environment impacts function.
Area of Science:
- Biochemistry
- Hematology
- Molecular Biology
Background:
- Platelets possess glycoprotein receptors, including glycoprotein Ib and the fibrinogen receptor alphaIIb betaIIIa.
- These receptors, particularly alphaIIb betaIIIa, contain redox-sensitive thiol groups and vicinal thiols.
- Protein disulfide isomerase (PDI) and other disulfide isomerases play a role in platelet aggregation.
Purpose of the Study:
- To explore the role of redox modification of platelet glycoproteins in platelet activation and aggregation.
- To investigate the influence of disulfide bond rearrangement in receptor signaling.
- To understand the impact of redox homeostasis in blood on platelet function.
Main Methods:
- Analysis of thiol and disulfide group modifications in platelet glycoproteins.
- Investigation of the role of protein disulfide isomerase (PDI) in platelet aggregation.
- Examination of the effects of various redox compounds (e.g., glutathione, nitric oxide) on platelet responsiveness.
Main Results:
- Dynamic disulfide bond rearrangement is essential for alphaIIb betaIIIa integrin structural changes during activation.
- The P2Y12 ADP receptor contains extracellular thiols susceptible to redox modification, influencing aggregation.
- Redox modulation by low molecular weight thiols and nitric oxide can alter platelet responsiveness.
Conclusions:
- Redox-sensitive thiols and disulfide bonds in platelet glycoproteins are critical for platelet function.
- A redox homeostasis likely exists in blood, analogous to pH or calcium regulation.
- Altering the platelet redox environment through disease or pharmacology significantly impacts platelet activity.
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