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Background: Endoplasmic reticulum (ER) stress is involved in the pathogenesis of atherosclerosis. Results: Pharmacological manipulation and siRNA treatment to reduce ER stress mitigate ox-LDL-induced CD36 up-regulation, which is promoted synergistically by ER stress inducer. Conclusion: ER stress promotes macrophage-derived foam cell formation by up-regulating CD36. Significance: ER stress-mediated macrophage-derived foam cell formation may be a novel target in the prevention of atherosclerosis.

Aim: This study was to explore whether activating transcription factor 6 (ATF6), an important sensor to endoplasmic reticulum (ER) stress, would mediate oxidized low-density lipoprotein (ox-LDL) -induced cholesterol accumulation and apoptosis in cultured macrophages and the underlying molecular mechanisms. Methods: Intracellular lipid droplets and total cholesterol levels were assayed by oil red O staining and enzymatic colorimetry, respectively. Cell viability and apoptosis were determined using MTT assay and AnnexinV-FITC apoptosis detection kit, respectively. The nuclear translocation of ATF6 in cells was detected by immunofluorescence analysis. Protein and mRNA levels were examined by Western blot analysis and real time-PCR, respectively. ATF6 siRNA was transfected to RAW264.7 cells by lipofectamin.

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