HDL (Human) ELISA Kit

Objective: LCAT (lecithin cholesterol acyltransferase) deficiency results in severe low HDL (high-density lipoprotein). Although whether LCAT is pro- or antiatherosclerosis was in debate in mouse studies, our previous study clearly shows that LCAT deficiency (LCAT(-/-)) in hamster accelerates atherosclerotic development on high-fat diet. However, unlike in hypercholesterolemia and hypertriglyceridemia, whether LCAT deficiency could lead to spontaneous atherosclerosis has not been studied yet in animal models. We, therefore, sought to investigate the atherosclerosis in LCAT(-/-) hamsters on standard laboratory diet and explore the potential underlying mechanisms. Approach and Results: Young (<8 months) and aged (>16 months) male and female wild-type and LCAT(-/-) hamsters on standard laboratory diet were used. Compared with age- and sex-matched wild-type hamsters, LCAT(-/-) hamsters showed a complete loss of plasma HDL and an increase in triglyceride by 2- to 8-fold at different stages of age. In aged LCAT(-/-) hamsters, the lesion areas at the aortic roots were approximate to 40x10(4) mu m(3) in males and 18x10(4) mu m(3) in females, respectively, which were consistent with the en face plaques observed in male (1.2%) and (1.5%) female groups, respectively. The results of plasma malondialdehyde measurement showed that malondialdehyde concentrations were markedly elevated to 54.4 mu mol/L in males and 30 mu mol/L in females, which are significantly associated with the atherosclerotic lesions. Conclusions: Our study demonstrates the development of spontaneous atherosclerotic lesions in aged male and female LCAT(-/-) hamsters with higher plasma oxidative lipid levels independent of plasma total cholesterol levels, further confirming the antiatherosclerotic role of LCAT.

Background: Adenosine triphosphate-binding cassette subfamily G member 1 (ABCG1) has the function of transporting free intracellular cholesterol to extracellular high-density lipoprotein (HDL) particles, which play a crucial role in atherosclerosis. The goal of this study is to examine the relationship between the polymorphisms of the ABCG1 gene promoter region and ischemic stroke. Methods: In the present study, a case-control association study was designed to identify 3 single-nucleotide polymorphisms (SNPs; rs5713919, rs1378577, and rs1893590), which were located in the promoter region of ABCG1 gene by kompetitive allele-specific polymerase chain reaction genotyping approach. The in vitro luciferase assay was done to estimate the effect of rs5713919 on gene expression. Finally, the relationships of 3 SNPs of ABCG1 gene with plasma lipids and lipoproteins were investigated in this Chinese cohort. Results: The correlation analysis between lipids and genotypes showed that the rs57137919 locus genotype was significantly associated with HDL cholesterol (HDL-C) and low-density lipoprotein cholesterol (LDL-C) levels (P = 0.021 and P = 0.017, respectively), and the GA and AA genotypes had higher HDL-C levels than the GG genotype. Conclusions: Our study provides evidence that ABCG1 promoter region polymorphism rs57137919 has an influence on plasma HDL-C and LDL-C levels in Chinese Han population.