Platelet Activation by Oxidized Low Density Lipoprotein Is Mediated by Cd36 and Scavenger Receptor-A

@article{Korporaal2007PlateletAB,
  title={Platelet Activation by Oxidized Low Density Lipoprotein Is Mediated by Cd36 and Scavenger Receptor-A},
  author={S. Korporaal and M. van Eck and J. Adelmeijer and M. Ijsseldijk and Ruud Out and T. Lisman and P. Lenting and T. V. van Berkel and J. Akkerman},
  journal={Arteriosclerosis, Thrombosis, and Vascular Biology},
  year={2007},
  volume={27},
  pages={2476-2483}
}
Objective—The interaction of platelets with low density lipoprotein (LDL) contributes to the development of cardiovascular disease. Platelets are activated by native LDL (nLDL) through apoE Receptor 2′ (apoER2′)-mediated signaling to p38MAPK and by oxidized LDL (oxLDL) through lysophosphatidic acid (LPA) signaling to Rho A and Ca2+. Here we report a new mechanism for platelet activation by oxLDL. Methods and Results—Oxidation of nLDL increases p38MAPK activation through a mechanism that is (1… Expand
Scavenger receptor A and CD36 are implicated in mediating platelet activation induced by oxidized low- density lipoproteins.
TLDR
It is shown very elegantly that oxLDL, in tandem with CD36 and SRA, is activating platelets and potentially increasing the risk of thrombosis and triggering a novel platelet-activating pathway triggered by partially oxidized LDL. Expand
A Specific CD36-Dependent Signaling Pathway Is Required for Platelet Activation by Oxidized Low-Density Lipoprotein
TLDR
It is shown that mitogen-activated protein kinase c-Jun N-terminal kinase (JNK)2 and its upstream activator MKK4 were phosphorylated in platelets exposed to oxLDL, suggesting that a specific CD36-dependent signaling pathway is required for platelet activation by ox LDL. Expand
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TLDR
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TLDR
It is demonstrated that oxLDL and hyperlipidemia stimulate the generation of NOX2-derived ROS through a CD36-PKC pathway and may promote platelet hyperactivity through modulation of cGMP signaling. Expand
Native High Density Lipoproteins (HDL) Interfere with Platelet Activation Induced by Oxidized Low Density Lipoproteins (OxLDL)
TLDR
The finding that HDL effectively competed with the binding of OxLDL to the platelet surface might contribute to their atheroprotective and antithrombotic properties. Expand
Oxidized low-density lipoproteins induce rapid platelet activation and shape change through tyrosine kinase and Rho kinase-signaling pathways.
TLDR
It is shown that oxLDL stimulate platelet activation through phosphorylation of the regulatory light chains of the contractile protein myosin IIa (MLC), and new signaling events downstream of CD36 that are critical in promoting platelet aggregation are revealed. Expand
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TLDR
The results on OxLDL-mediated platelet–monocyte aggregate formation, which promoted phenotypic changes in monocytes, monocyte extravasation and enhanced foam cell formation in vitro and in vivo, provide a novel mechanism for how platelets potentiate key steps of atherosclerotic plaque development and plaque destabilization. Expand
Regulation of Platelet Function by Class B Scavenger Receptors in Hyperlipidemia
  • A. Zimman, E. Podrez
  • Biology, Medicine
  • Arteriosclerosis, thrombosis, and vascular biology
  • 2010
TLDR
It is demonstrated that platelet class B scavenger receptors play roles in thrombosis in dyslipidemia and may contribute to acute cardiovascular events in vivo in hypercholesterolemia. Expand
Platelet Activation by Low Concentrations of Intact Oxidized LDL Particles Involves the PAF Receptor
TLDR
Intact oxLDL particles activate platelets through the PAf receptor, and the PAF receptor responds to a far wider range of oxidized phospholipids in oxLDl than anticipated. Expand
Atherogenic lipid stress induces platelet hyperactivity through CD36-mediated hyposensitivity to prostacyclin: the role of phosphodiesterase 3A
TLDR
CD36 can translate atherogenic lipid stress into platelet hyperactivity through modulation of inhibitory cAMP signaling, and genetic deletion of CD36 protected dyslipidemic animals from PGI2 hyposensitivity and restored PKA signaling. Expand
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References

SHOWING 1-10 OF 54 REFERENCES
Binding of Low Density Lipoprotein to Platelet Apolipoprotein E Receptor 2′ Results in Phosphorylation of p38MAPK *
TLDR
The data indicate that apoER2′ contributes to LDL-dependent sensitization of platelets, a kinase that is able to activate p38MAPK. Expand
Effect of Oxidation on the Platelet-Activating Properties of Low-Density Lipoprotein
TLDR
At >30% oxidation, LDL interferes with ligand binding to integrin &agr;IIb&bgr;3, thereby attenuating platelet functions. Expand
Platelet Endothelial Cell Adhesion Molecule-1 (PECAM-1) Inhibits Low Density Lipoprotein-induced Signaling in Platelets*
TLDR
This work reports that the transient nature of p38MAPK activation is caused by platelet endothelial cell adhesion molecule 1 (PECAM-1), a receptor with an immunoreceptor tyrosine-based inhibitory motif, and suggests that, following a first phase in which LDL, through its B-site, phosphorylates and thereby activates p38 MAPK, a second phase is initiated. Expand
Early platelet activation by low density lipoprotein via p38MAP kinase.
TLDR
Activation of p38MAPK might be the first step in platelet sensitization by LDL, leading to formation of arachidonate metabolites and increased aggregation and secretion responses to physiological agonists. Expand
Low-Density Lipoprotein Enhances Platelet Secretion Via Integrin-αIIbβ3–Mediated Signaling
Abstract —LDL is known to increase the sensitivity of human platelets for agonists and to induce aggregation and secretion independently at high concentrations, but its mechanism of action is largelyExpand
Mildly Oxidized Low Density Lipoprotein Rapidly Stimulates via Activation of the Lysophosphatidic Acid Receptor Src Family and Syk Tyrosine Kinases and Ca2+ Influx in Human Platelets*
TLDR
The results indicate that mox-LDL, through activation of the LPA receptor, stimulates two separate early signal pathways, (a) Src family and Syk tyrosine kinases, and (b) Ca2+ entry, which probably plays a role in platelet responses subsequent to shape change. Expand
Lysophosphatidic acid mediates the rapid activation of platelets and endothelial cells by mildly oxidized low density lipoprotein and accumulates in human atherosclerotic lesions.
TLDR
This study identifies LPA as an atherothrombogenic molecule and suggests a possible strategy to prevent and treat atherosclerosis and cardiocerebrovascular diseases. Expand
Platelet activation by oxidatively modified low density lipoproteins.
TLDR
The data suggest that activation of platelet responses results from changes in membrane fluidity, which shed new light on the potential role of altered lipoproteins in the pathogenesis of atherosclerosis and its complications. Expand
Subtype-Selective Antagonists of Lysophosphatidic Acid Receptors Inhibit Platelet Activation Triggered by the Lipid Core of Atherosclerotic Plaques
TLDR
LPA molecules present in the core region of atherosclerotic plaques trigger rapid platelet activation through the stimulation of LPA1 and LPA3 receptors, and antagonists of platelet LPA receptors might provide a new strategy to prevent thrombus formation in patients with cardiovascular diseases. Expand
Mildly oxidized LDL induces platelet aggregation through activation of phospholipase A2.
TLDR
Results indicate that mildly oxidized LDL activates platelets through a phospholipase A2/cyclooxygenase-dependent pathway and the complete inhibition of mox-LDL-induced platelet aggregation by aspirin could contribute to its beneficial effect in cardiovascular disease. Expand
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