December 27, 2006The FASEB Journal
LDL are oxidatively modified by platelets via GP91 phox and accumulate in human monocytes
Key result
Collagen-stimulated platelets induced LDL modification via NADPH oxidase-mediated oxidative stress, an effect enhanced in hypercholesterolemia and reduced in gp91phox deficiency.
Why the study?
Do human platelets oxidatively modify LDL via NADPH oxidase-mediated oxidative stress?
Population
Human platelets taken from healthy subjects, patients with hereditary deficiency of gp91phox, and patients…
Comparison
Incubation with LDL and stimulation with… vs Unstimulated platelets; platelets from healthy…
Design
Preclinical
Authors
Discussion
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Member takes
Implication
May implicate platelets in LDL oxidation within plaques; hypothesis-generating in animals, human studies needed before clinical relevance.
Structured PICO
Do human platelets oxidatively modify LDL via NADPH oxidase-mediated oxidative stress?
P
Population
Human platelets from healthy subjects, patients with hereditary deficiency of gp91phox, and patients with hypercholesterolemia.
E
Exposure
Incubation with LDL and stimulation with collagen; treatment with arachidonyl trifluomethyl ketone (AACOCF3)
C
Comparator
Unstimulated platelets; platelets from healthy subjects
O
Outcome
LDL oxidative modification (measured by conjugated dienes, lysophosphatidylcholine formation, electrophoretic mobility, Apo B-100 degradation, monocyte LDL uptake, and vitamin E reduction)surrogate
Platelets modify LDL via NADPH oxidase-mediated oxidative stress, suggesting a role for platelets in promoting LDL accumulation within atherosclerotic plaques.
Cite This Study
Carnevale et al. (2006) studied Hypercholesterolemia, hereditary deficiency of gp91phox. Collagen stimulation vs. Unstimulated platelets was evaluated on LDL modification. Collagen-stimulated platelets induced LDL modification via NADPH oxidase-mediated oxidative stress, an effect enhanced in hypercholesterolemia and reduced in gp91phox deficiency.