Key Points
- To determine whether CD36 mediates very low-density lipoprotein (VLDL)-induced platelet activation and enhanced aggregation.
- Measured platelet aggregation lag time, maximal aggregation, and thromboxane A2 generation in response to collagen with or without VLDL exposure.
- Inhibited CD36 function using a monoclonal antibody and validated receptor specificity by testing platelets isolated from Cd36-deficient versus wild-type rats.
- VLDL enhanced collagen-induced platelet activation by shortening aggregation lag time to 70% of control (P = 0.001), increasing maximum aggregation to 170% of control (P = 0.008), and elevating thromboxane production to 3,318% of control (P = 0.004).
- CD36 monoclonal antibody treatment blocked VLDL binding by 75% (P = 0.041), prolonged aggregation lag time to 190% (P < 0.001), and reduced thromboxane production to 8% of control (P < 0.001), with Cd36-deficient rat platelets exhibiting no VLDL-enhanced activation.
Structured PICO
Does CD36 mediate VLDL-enhanced platelet activation and aggregation?
PPopulationIn vitro platelets and platelets from Cd36-deficient rats versus rats expressing CD36
IInterventionVLDL exposure and monoclonal antibody against CD36
CComparatorControl platelets stimulated with collagen
OOutcomeCollagen-mediated platelet aggregation (lag time and maximum aggregation) and thromboxane A2 productionsurrogate
The platelet CD36 receptor plays a key mechanistic role in VLDL-induced platelet activation, providing a potential link between diabetic dyslipidemia and atherothrombosis.