Platelet activation by low density lipoprotein and high density lipoprotein.
Cardiovascular disease is the main cause of death and disability in the Western society. Lipoproteins are important in the development of cardiovascular disease since they change the properties of different cells involved in atherosclerosis and thrombosis. The interaction of platelets with lipoproteins has been under intense investigation. Particularly the initiation of platelet signaling pathways by low density lipoprotein (LDL) has been studied thoroughly, since platelets of hypercholesterolemic patients, whose plasma contains elevated LDL levels due to absent or defective LDL receptors, show hyperaggregability in vitro and enhanced activity in vivo. These observations suggest that LDL enhances platelet responsiveness. Several signaling pathways induced by LDL have been revealed in vitro, such as signaling via p38 mitogen-activated protein kinase and p125 focal adhesion kinase. High density lipoprotein (HDL) consists of two subtypes, HDL(2) and HDL(3), which have opposing effects on platelet activation. This review provides a summary of the activation of signaling pathways after platelet-LDL and platelet-HDL interaction, with special emphasis on their role in the development of thrombosis and atherosclerosis.
Korporaal
Suzanne J A
SJ
Thrombosis and Haemostasis Laboratory, Department of Haematology, University Medical Center Utrecht and The Institute for Biomembranes, University of Utrecht, The Netherlands. j.a.korporaal@azu.nl
Akkerman
Jan-Willem N
JW
D050197:Atherosclerosis / Q000209:etiology; D008076:Cholesterol, HDL / Q000145:classification / Q000502:physiology*; D008078:Cholesterol, LDL / Q000145:classification / Q000502:physiology*; D006801:Humans; D008954:Models, Biological; D015539:Platelet Activation / Q000502:physiology*; D015398:Signal Transduction; D013927:Thrombosis / Q000209:etiology
D008076:Cholesterol, HDL; D008078:Cholesterol, LDL