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To investigate the effect of CML on the migration of foam cells.
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.
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 . Wound scratch assay and modified boyden chamber migration assay demonstrated that CML significantly inhibits the migration of RAW264.7 macrophages (p<0.05), By inhibiting the CD36 / Vav1 pathway, this process can be alleviated.
CML could inhibit the migration of RAW264.7-derived foam cells via CD36/Vav1 pathway.