Key result
Addition of hypochlorite-oxidized HDL to human platelets resulted in an immediate, dose-dependent increase in intracellular calcium, P-selectin expression, and platelet aggregation.
Why the study?
Does hypochlorite-oxidized HDL increase platelet reactivity in human platelets?
Does hypochlorite-oxidized HDL increase platelet reactivity in human platelets?
Oxidation of HDL by hypochlorite converts it from a protective factor into a potent platelet agonist via the CD36 receptor, providing a mechanistic link to cardiovascular disease.
Answers are grounded in this paper and cite their sources.
Should not yet change practice; leaves open oxidized HDL as a platelet agonist in cardiovascular disease.
High density lipoproteins (HDL) represent a protective factor of central importance that counteracts the development of cardiovascular disease, in part by normalizing platelet (hyper)reactivity. As HDL represent an efficient scavenger of the naturally occurring oxidant hypochlorite, this work was intended to investigate the influence of hypochlorite-oxidized HDL on platelet function. Addition of hypochlorite-oxidized HDL to human platelets results in an immediate and transient raise in intracellular calcium, surface expression of P-selectin and platelet aggregation. The observed effects are dose dependent and can be blocked by an antibody directed against the lipoprotein-binding domain of platelet thrombospondin- and scavenger receptor CD36.
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Assinger et al. (2008) studied this question. Hypochlorite-oxidized HDL was evaluated on Intracellular calcium, surface expression of P-selectin and platelet aggregation. Addition of hypochlorite-oxidized HDL to human platelets resulted in an immediate, dose-dependent increase in intracellular calcium, P-selectin expression, and platelet aggregation.
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