Apolipoprotein E mRNA expression in mononuclear cells from normolipidemic and hypercholesterolemic individuals treated with atorvastatin

<p>Abstract</p> <p>Background</p> <p>Apolipoprotein E (apoE) is a key component of the lipid metabolism. Polymorphisms at the apoE gene (<it>APOE</it>) have been associated with cardiovascular disease, lipid levels and lipid-lowering response to statins. We evaluated the effects on <it>APOE </it>expression of hypercholesterolemia, <it>APOE </it>ε2/ε3/ε4 genotypes and atorvastatin treatment in Brazilian individuals. The relationship of <it>APOE </it>genotypes and plasma lipids and atorvastatin response was also tested in this population.</p> <p>Methods</p> <p><it>APOE </it>ε2/ε3/ε4 and plasma lipids were evaluated in 181 normolipidemic (NL) and 181 hypercholesterolemic (HC) subjects. HC individuals with indication for lowering-cholesterol treatment (n = 141) were treated with atorvastatin (10 mg/day/4-weeks). <it>APOE </it>genotypes and <it>APOE </it>mRNA in peripheral blood mononuclear cells (PBMC) were analyzed by TaqMan real time PCR.</p> <p>Results</p> <p>HC had lower <it>APOE </it>expression than NL group (p < 0.05) and individuals with low <it>APOE </it>expression showed higher plasma total and LDL cholesterol and apoB, as well as higher apoAI (p < 0.05). Individuals carrying ε2 allele have reduced risk for hypercholesterolemia (OR: 0.27, 95% I.C.: 0.08-0.85, p < 0.05) and NL ε2 carriers had lower total and LDL cholesterol and apoB levels, and higher HDL cholesterol than non-carriers (p < 0.05). <it>APOE </it>genotypes did not affect <it>APOE </it>expression and atorvastatin response. Atorvastatin treatment do not modify <it>APOE </it>expression, however those individuals without LDL cholesterol goal achievement after atorvastatin treatment according to the IV Brazilian Guidelines for Dyslipidemia and Atherosclerosis Prevention had lower <it>APOE </it>expression than patients with desirable response after the treatment (p < 0.05).</p> <p>Conclusions</p> <p><it>APOE </it>expression in PBMC is modulated by hypercholesterolemia and the <it>APOE </it>mRNA level regulates the plasma lipid profile. Moreover the expression profile is not modulated neither by atorvastatin nor <it>APOE </it>genotypes. In our population, <it>APOE </it>ε2 allele confers protection against hypercholesterolemia and a less atherogenic lipid profile. Moreover, low <it>APOE </it>expression after treatment of patients with poor response suggests a possible role of <it>APOE </it>level in atorvastatin response.</p>

Abstract licence: CC BY-NC-ND

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