Abstract: Targeting DNA methylation modifications at specific genes has emerged as a potential strategy to ameliorate atherosclerosis development, but little is known about the relationship of methylases with macrophage foam cell formation. In this study, 5-aza-2-deoxycytidine(5-Aza) was used to treat primary mouse peritoneal macrophages collected, and the macrophage foam cell formation and inflammatory factors expression were determined. Then CD36 siRNA was used to interfere with the CD36 expression of macrophage J774 and RAW264.7 cells, and the peritoneal macrophages of macrophage specific peroxisome proliferator activated receptor(PPARγ) knockout mice were extracted to study the role and mechanism of 5-Aza in regulating macrophage foam cell formation. The results revealed that 5-Aza promoted macrophage foam cell formation by enhancing macrophage CD36 expression, membrane localization, and mRNA levels, but 5-Aza had little effect on CD36 levels in PPARγ knockout macrophages. The results suggest that 5-Aza can promote macrophage foam cell formation by enhancing the expression of CD36, which is mediated by PPARγ. This study also illustrates the new function of 5-Aza and may provide new strategy for prevention and treatment of atherosclerosis.
Keywords: 5-aza-2-deoxycytidine(5-Aza); CD36; macrophage foam cell formation; PPAR $ \gamma $; inflammatory factor
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