Figure 1
Figure 1. AGE bind to platelets via CD36. (A) Isolated wt or cd36-null platelets were washed and incubated at 22°C with different concentrations of biotin-AGE-BSA or biotin-BSA as controls for 2 hours, followed by avidin-Alexa Fluor 488 conjugate treatment for 1 hour. Platelets were then analyzed by flow cytometry to detect bound fluorescence. The histogram shown is representative of 3. (B) Increasing concentrations of AGE-BSA were added to wt or cd36-null platelets in the presence of either NO2+LDL or NO2−LDL (100 μg/mL). Bound fluorescence was detected as in panel A. (C) Wells in a 96-well ELISA plate were coated with recombinant CD36-MBP fusion protein or MBP (25 μg/mL in PBS) at 4°C overnight. Increasing concentrations of AGE-BSA were then added for 2 hours at 22°C, and bound material was detected with anti-AGE using a colorimetric ELISA assay. Data are presented as the mean fold change from control (± SEM); n = 3.

AGE bind to platelets via CD36. (A) Isolated wt or cd36-null platelets were washed and incubated at 22°C with different concentrations of biotin-AGE-BSA or biotin-BSA as controls for 2 hours, followed by avidin-Alexa Fluor 488 conjugate treatment for 1 hour. Platelets were then analyzed by flow cytometry to detect bound fluorescence. The histogram shown is representative of 3. (B) Increasing concentrations of AGE-BSA were added to wt or cd36-null platelets in the presence of either NO2+LDL or NO2LDL (100 μg/mL). Bound fluorescence was detected as in panel A. (C) Wells in a 96-well ELISA plate were coated with recombinant CD36-MBP fusion protein or MBP (25 μg/mL in PBS) at 4°C overnight. Increasing concentrations of AGE-BSA were then added for 2 hours at 22°C, and bound material was detected with anti-AGE using a colorimetric ELISA assay. Data are presented as the mean fold change from control (± SEM); n = 3.

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