RESUMO
Background: there is evidence that CD36 promotes foam cell formation through internalizing oxidized LDL [ox- LDL] into macrophages; therefore, it plays a key role in pathogenesis of atherosclerosis. In addition, CD36 expression seems to be mediated by nuclear receptor peroxisome proliferator-activated receptor gamma [PPAR-[gamma]]. The aim of the present study was to evaluate and compare the effect of PPAR-[gamma] ligands, eicosapentaenoic acid [EPA] as an anti-atherogenic factor and ox-LDL as an atherogenic factor on CD36 expression. Mechanism of PPAR-[gamma] action and its ligands in CD36 expression were also investigated
Methods: raw 264.7 macrophage cell line was treated with ox-LDL [100 and 150 [micro]g protein/LDL] and EPA [100 and 200 [micro]M] for 24 and 48 hours in absence or presence of PPAR-[gamma] inhibitor, T0070907. Quantitative real-time PCR and Western-blotting were used for analysis of gene and protein expression, respectively
Results: raw 264.7 exposures to ox-LDL and EPA resulted in increased expression of CD36 mRNA and protein; however, mRNA and PPAR-[gamma] protein were not upregulated significantly. Pre-incubation of cells with T0070907 led to decreased expression of CD36 when treated with ox-LDL and EPA
Conclusion: it was confirmed that both EPA and ox-LDL increased CD36 expression but not PPAR-[gamma], and also co-treatment with PPAR-[gamma] inhibitor decreased CD36 expression. We concluded that upregulation of CD36 depends on PPAR-[gamma] activation and is not related to increased expression of PPAR-[gamma]. Induction of CD36 by EPA showed that CD36 suppression is not the means by which [omega]-3 fatty acids [EPA] provide protection against formation of atherosclerotic plaque. Iran. Biomed. J. 17 [2]: 84-92, 2013