Oxysterols and TBARS are among the LDL oxidation products which enhance thromboxane A2 synthesis by platelets

Mahfouz, Mahmoud; Kummerow, F.A.

doi:10.1016/s0090-6980(98)00056-2

Cited by 17 publications

(4 citation statements)

References 57 publications

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“…Partially hydrogenated soybean oil contained 14 cis and trans isomers that were formed during hydrogenation [4,5]. They inhibited cyclooxygenase, an enzyme required for the conversion of arachidonic acid to prostacyclin, a molecule which prevents blood clots [43]. Moreover, oxidized fat enhanced thromboxane synthesis [44,45], which caused the formation of a blood clot.…”

Section: The Trans Fatty Acids In Partially Hydrogenated Fat Can Causmentioning

confidence: 99%

The Effects of Hydrogenation on Soybean Oil

Kummerow¹

2013

Soybean - Bio-Active Compounds

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Section: The Trans Fatty Acids In Partially Hydrogenated Fat Can Causmentioning

confidence: 99%

The Effects of Hydrogenation on Soybean Oil

Kummerow¹

2013

Soybean - Bio-Active Compounds

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“…The presence of thromboxane, a potent inducer of vasoconstriction and platelet adhesion, in the arteries is partially responsible for the interruption of blood flow, causing the clogging of the arteries [12]. The components of oxLDL were responsible for platelet sensitization to thrombin and the increase of thromboxane release.…”

Section: With Permission Of the University Of Illinois And The Carle mentioning

confidence: 99%

The Cause for Heart Disease and Strokes

Kummerow¹

2013

J. Nutr. Ther.

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There has been no solution to heart disease to date. I obtained discarded veins from bypass (CABG) surgeries and subjected them to phospholipid analysis. We also obtained arterial cells from human umbilical cords and cultured them with a decreasing concentration of either cholesterol or oxidized cholesterol. Patients undergoing CABG surgery and aging swine had significantly higher levels of sphingomyelin in their arterial cells than arterial cells from human umbilical cords. Oxidized low-density lipoprotein (OxLDL) and oxysterols further contribute to atherosclerosis by increasing the synthesis of thromboxane in platelets, a clotting factor. When we incubated arterial cells with cholesterol that had not been oxidized, even at twelve times the concentration of the oxidized cholesterols we used, there was no effect on sphingomyelin content, this shows that cholesterol itself is not the reason for heart disease, and has to be oxidized in order to cause harm. My study indicated that atherosclerosis is due to a diet that contains a high level of oxysterols. Normal levels of oxysterols in the plasma will not increase sphingomyelin levels. Removing oxidized fat from the diet should be considered as a therapeutic measure for atherosclerosis. Ancel Keys, who some consider the father of the cholesterol-heart disease hypothesis said in 1997: "There's no connection whatsoever between the cholesterol in food and cholesterol in the blood."

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“…Signaling pathways induced by oxLDL in platelets include activation of Rho/Rho kinase 56 and Src-family and Syk tyrosine kinases 57–58. A number of recent studies provided evidence of the signaling events initiated by oxLDL in platelets and mediated by CD36.…”

Section: Platelet Cd36 Oxidized Phospholipids and Thrombosismentioning

confidence: 99%

“…However, it should be mentioned that a complex ligand such as oxidized LDL contains multiple biologically active components that can affect platelet function in a CD36 independent manner. Examples include oxidized lipids that increase intracellular Ca 2+ through the PAF receptor64, lysophosphatidylcholine65, oxysterols and TBARS58, lysophosphatydic acid66 and amyloid-like structures 46.…”

Section: Platelet Cd36 Oxidized Phospholipids and Thrombosismentioning

confidence: 99%

Regulation of Platelet Function by Class B Scavenger Receptors in Hyperlipidemia

Zimman

Podrez

2010

ATVB

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Abstract-Platelets constitutively express class B scavenger receptors CD36 and SR-BI, 2 closely related pattern recognition receptors best known for their roles in lipoprotein and lipid metabolism. The biological role of scavenger receptors in platelets is poorly understood. However, in vitro and in vivo data suggest that class B scavenger receptors modulate platelet function and contribute significantly to thrombosis by sensing pathological or physiological ligands, inducing prothrombotic signaling, and increasing platelet reactivity. Platelet CD36 recognizes a novel family of endogenous oxidized choline phospholipids that accumulate in plasma of hyperlipidemic mice and in plasma of subjects with low high-density lipoprotein levels. This interaction leads to the activation of specific signaling pathways and promotes platelet activation and thrombosis. Platelet SR-BI, on the other hand, plays a critical role in the induction of platelet hyperreactivity and accelerated thrombosis under conditions associated with increased platelet cholesterol content. Intriguingly, oxidized high-density lipoprotein, an SR-BI ligand, can suppress platelet function. These recent findings demonstrate that platelet class B scavenger receptors play roles in thrombosis in dyslipidemia and may contribute to acute cardiovascular events in vivo in hypercholesterolemia. Key Words: lipids Ⅲ lipoproteins Ⅲ oxidized lipids Ⅲ platelets Ⅲ signal transduction S cavenger receptors (SR) are a group of structurally heterologous cell surface receptors that share an ability to recognize chemically modified or oxidized forms of lowdensity lipoprotein (LDL). SR belong to a wider family of pattern recognition receptors that mediate the innate immune host response which includes Toll-like receptors. Platelets express several SR including class B SR CD36 and SR-BI, 2 closely related multiligand receptors, best known for their roles in lipoprotein and lipid metabolism. 1 Other platelet SR include LOX-1 and CD68. 1 Expression of class B SR in platelets is mainly constitutive, whereas other receptors are rapidly exposed on platelet activation. Ligands for these receptors can be roughly divided into 3 groups: physiological ligands, pathological endogenous (changed self) ligands, and pathological exogenous ligands. Pathological endogenous ligands for platelet SR may be present in circulation in a number of pathophysiological states related to dyslipidemia and oxidative stress. Pathological exogenous ligands may be present in cases of infections. The biological role of SR in platelets is not understood yet. However, evidence is accumulating that SR contribute significantly to thrombosis by sensing pathological or physiological ligands, inducing prothrombotic signaling, and increasing platelet reactivity. This in turn may lead to thrombosis in the presence of threshold concentrations of agonists. Platelet hyperreactivity or increased platelet response to agonists is associated with augmented platelet adhesion, integrin activation, and aggregation. [2][3][4] Subj...

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Oxysterols and TBARS are among the LDL oxidation products which enhance thromboxane A2 synthesis by platelets

Cited by 17 publications

References 57 publications

The Effects of Hydrogenation on Soybean Oil

The Effects of Hydrogenation on Soybean Oil

The Cause for Heart Disease and Strokes

Regulation of Platelet Function by Class B Scavenger Receptors in Hyperlipidemia

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