Compare the effect of eicosapentaenoic acid and Ooxidized Low- density lipoprotein on the expression of CD36 and peroxisome proliferator-activated receptor gamma

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

Cloning of coagulant VII factor from hepatoma cell line

Factor VII, is a coagulant protease; it begins the proteolytic cascade reactions and produces thrombin. The use of recombinant human factor VII, [rhFVII] is effective for the treatment of patients with hemophilia A or B. It is a target for gene therapy. This study was done to clone factor VII from HepG2 cell line. RNA was extracted from the hepatoma, [HepG2], cell line. On reverse transcription FVII cDNA was amplified by RT-PCR. PCR product was cloned into the pTZ57R/T vector and transported into the E-coli cells. By amplification of the FVII gene, the PCR band was observed and cloning into the vector was confirmed by restriction analysis. In this paper we report the cloning of factor VII from HepG2 cell line