Abstract

The intracellular mechanisms underlying oxidized low density lipoprotein (oxLDL)-signaling pathways in platelets remain obscure and findings have been controversial. Therefore, we examined the influence of oxLDL in washed human platelets. In this study, oxLDL concentration-dependently (20-100 μg/mL) inhibited platelet aggregation in human platelets stimulated by collagen (1 μg/mL) and arachidonic acid (60 μM), but not by thrombin (0.02 U/mL). The activity of oxLDL was greater at 24 h in inhibiting platelet aggregation than at 12 h. At 24 h, oxLDL concentration-dependency inhibited intracellular Ca 2+ mobilization and thromboxane B2 formation in human platelets stimulated by collagen. In addition, at 24 h oxLDL (40 and 80 μg/mL) significantly increased the formation of cyclic AMP, but not cyclic GMP or nitrate. In an ESR study, 24 h-oxLDL (40 μg/mL) markedly reduced the ESR signal intensity of hydroxyl radicals (OH-) in both collagen (2 μg/mL)-activated platelets and Fenton reaction (H2O2 + Fe2+). The inhibitory effect of oxLDL may induce radical-radical termination reactions by oxLDL-derived lipid radical interactions with free radicals (such as hydroxyl radicals) released from activated platelets, with a resultant lowering of intracellular Ca2+ mobilization, followed by inhibition of thromboxane A2 formation, thereby leading to increased cyclic AMP formation and finally inhibited platelet aggregation. This study provides new insights concerning the effect of oxLDL in platelet aggregation.

Original languageEnglish
Pages (from-to)433-440
Number of pages8
JournalLipids
Volume39
Issue number5
DOIs
Publication statusPublished - May 2004

Fingerprint

low density lipoprotein
Platelets
Blood Platelets
platelet aggregation
Platelet Aggregation
Agglomeration
collagen
thromboxanes
Collagen
cyclic AMP
hydroxyl radicals
Hydroxyl Radical
Cyclic AMP
Paramagnetic resonance
oxidized low density lipoprotein
In Vitro Techniques
cyclic GMP
Thromboxane B2
Thromboxane A2
thrombin

ASJC Scopus subject areas

  • Medicine (miscellaneous)
  • Biochemistry, Genetics and Molecular Biology(all)
  • Food Science
  • Biochemistry

Cite this

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title = "Low concentration of oxidized low density lipoprotein suppresses platelet reactivity in vitro: An intracellular study",
abstract = "The intracellular mechanisms underlying oxidized low density lipoprotein (oxLDL)-signaling pathways in platelets remain obscure and findings have been controversial. Therefore, we examined the influence of oxLDL in washed human platelets. In this study, oxLDL concentration-dependently (20-100 μg/mL) inhibited platelet aggregation in human platelets stimulated by collagen (1 μg/mL) and arachidonic acid (60 μM), but not by thrombin (0.02 U/mL). The activity of oxLDL was greater at 24 h in inhibiting platelet aggregation than at 12 h. At 24 h, oxLDL concentration-dependency inhibited intracellular Ca 2+ mobilization and thromboxane B2 formation in human platelets stimulated by collagen. In addition, at 24 h oxLDL (40 and 80 μg/mL) significantly increased the formation of cyclic AMP, but not cyclic GMP or nitrate. In an ESR study, 24 h-oxLDL (40 μg/mL) markedly reduced the ESR signal intensity of hydroxyl radicals (OH-) in both collagen (2 μg/mL)-activated platelets and Fenton reaction (H2O2 + Fe2+). The inhibitory effect of oxLDL may induce radical-radical termination reactions by oxLDL-derived lipid radical interactions with free radicals (such as hydroxyl radicals) released from activated platelets, with a resultant lowering of intracellular Ca2+ mobilization, followed by inhibition of thromboxane A2 formation, thereby leading to increased cyclic AMP formation and finally inhibited platelet aggregation. This study provides new insights concerning the effect of oxLDL in platelet aggregation.",
author = "Chou, {Duen Suey} and George Hsiao and Shen, {Ming Yi} and Fong, {Tsorng Harn} and Lin, {Chien Huang} and Tzeng-Fu Chen and Sheu, {Joen Rong}",
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T1 - Low concentration of oxidized low density lipoprotein suppresses platelet reactivity in vitro

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AU - Chou, Duen Suey

AU - Hsiao, George

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AU - Lin, Chien Huang

AU - Chen, Tzeng-Fu

AU - Sheu, Joen Rong

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N2 - The intracellular mechanisms underlying oxidized low density lipoprotein (oxLDL)-signaling pathways in platelets remain obscure and findings have been controversial. Therefore, we examined the influence of oxLDL in washed human platelets. In this study, oxLDL concentration-dependently (20-100 μg/mL) inhibited platelet aggregation in human platelets stimulated by collagen (1 μg/mL) and arachidonic acid (60 μM), but not by thrombin (0.02 U/mL). The activity of oxLDL was greater at 24 h in inhibiting platelet aggregation than at 12 h. At 24 h, oxLDL concentration-dependency inhibited intracellular Ca 2+ mobilization and thromboxane B2 formation in human platelets stimulated by collagen. In addition, at 24 h oxLDL (40 and 80 μg/mL) significantly increased the formation of cyclic AMP, but not cyclic GMP or nitrate. In an ESR study, 24 h-oxLDL (40 μg/mL) markedly reduced the ESR signal intensity of hydroxyl radicals (OH-) in both collagen (2 μg/mL)-activated platelets and Fenton reaction (H2O2 + Fe2+). The inhibitory effect of oxLDL may induce radical-radical termination reactions by oxLDL-derived lipid radical interactions with free radicals (such as hydroxyl radicals) released from activated platelets, with a resultant lowering of intracellular Ca2+ mobilization, followed by inhibition of thromboxane A2 formation, thereby leading to increased cyclic AMP formation and finally inhibited platelet aggregation. This study provides new insights concerning the effect of oxLDL in platelet aggregation.

AB - The intracellular mechanisms underlying oxidized low density lipoprotein (oxLDL)-signaling pathways in platelets remain obscure and findings have been controversial. Therefore, we examined the influence of oxLDL in washed human platelets. In this study, oxLDL concentration-dependently (20-100 μg/mL) inhibited platelet aggregation in human platelets stimulated by collagen (1 μg/mL) and arachidonic acid (60 μM), but not by thrombin (0.02 U/mL). The activity of oxLDL was greater at 24 h in inhibiting platelet aggregation than at 12 h. At 24 h, oxLDL concentration-dependency inhibited intracellular Ca 2+ mobilization and thromboxane B2 formation in human platelets stimulated by collagen. In addition, at 24 h oxLDL (40 and 80 μg/mL) significantly increased the formation of cyclic AMP, but not cyclic GMP or nitrate. In an ESR study, 24 h-oxLDL (40 μg/mL) markedly reduced the ESR signal intensity of hydroxyl radicals (OH-) in both collagen (2 μg/mL)-activated platelets and Fenton reaction (H2O2 + Fe2+). The inhibitory effect of oxLDL may induce radical-radical termination reactions by oxLDL-derived lipid radical interactions with free radicals (such as hydroxyl radicals) released from activated platelets, with a resultant lowering of intracellular Ca2+ mobilization, followed by inhibition of thromboxane A2 formation, thereby leading to increased cyclic AMP formation and finally inhibited platelet aggregation. This study provides new insights concerning the effect of oxLDL in platelet aggregation.

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