GW28-e0436 CML inhibits foam cells migration via CD36/Vav1 pathway

Methods Foam cells were made by RAW 264.7 macrophages with oxLDL for 24 h. RAW 264.7 macrophages were divided into five groups: control group (RAW264.7 macrophages), oxLDL group (RAW 264.7 macrophages + 40 μg/mL oxLDL), CML group (RAW 264.7 macrophages + 40 μg/mL oxLDL+ 10 μmol/L CML), CD36 knock down group (RAW 264.7 macrophages + 40 μg/mL oxLDL+ 10 μmol/L CML+CD36 siRNA) and Vav1 knock down group (RAW 264.7 macrophages + 40 μg/mL oxLDL+ 10 μmol/L CML+Vav1 siRNA).Cholesterol ester measurement, oil red O staining, wound scratch assay, modified boyden chamber migration assay, western blot analysis and immunofluorescence staining were then performed. Results Western blot analysis and immunofluorescence staining indicated that CML could efficiently up-regulate the expression of CD36 and p-Vav1.Oil red O staining and cholesterol ester measurement suggested that CML could dramatically induce RAW 264.7 macrophages transdifferentiating into foam cells and CD36 and Vav1 knock down group show that inhabitation of CD36/Vav1 pathway can reverse this process .