scholarly journals Genetic analysis of a polymorphism in the human apolipoprotein A-I gene promoter: effect on plasma HDL-cholesterol levels.

1994 ◽  
Vol 35 (7) ◽  
pp. 1292-1296
Author(s):  
D E Barre ◽  
R Guerra ◽  
R Verstraete ◽  
Z Wang ◽  
S M Grundy ◽  
...  
1996 ◽  
Vol 16 (12) ◽  
pp. 1424-1429 ◽  
Author(s):  
Nicolas Duverger ◽  
Céline Viglietta ◽  
Laurence Berthou ◽  
Florence Emmanuel ◽  
Anne Tailleux ◽  
...  

Human apolipoprotein A-I (apo A-I) transgenic rabbits were created by use of an 11-kb genomic human apo A-I construct containing a liver-specific promoter. Five independent transgenic lines were obtained in which human apo A-I gene had integrated and was expressed. Plasma levels of human apo A-I ranged from 8 to 100 mg/dL for the founder and up to 175 mg/dL for the progeny. Rabbit apo A-I levels were substantially decreased in the transgenic rabbits. HDL cholesterol (HDL-C) levels were higher in two of the five transgenic rabbit lines than in controls (line 20 versus nontransgenic littermate, HDL-C=80±7 versus 37±6 mg/dL; line 8 versus nontransgenic littermate, HDL-C=54±16 versus 35±6 mg/dL). This resulted in less atherogenic lipoprotein profiles, with very low (VLDL+LDL-C)/HDL-C ratios. HDL size and protein and lipid compositions were similar between transgenic and littermate nontransgenic rabbits. However, a large amount of pre-β apo A-I–containing lipoproteins was observed in the plasma of the highest human apo A-I expressor. Cell cholesterol efflux was evaluated with the incubation of whole serum from transgenic and control rabbits. Cell cholesterol efflux was highly correlated with HDL cholesterol, with apo A-I, and with the presence of pre-β apo A-I–containing lipoproteins. These rabbits will be an extremely useful model for the evaluation of the effect of increased hepatic apo A-I expression on atherosclerosis.


1990 ◽  
Vol 31 (8) ◽  
pp. 1371-1377
Author(s):  
F Pagani ◽  
A Sidoli ◽  
GA Giudici ◽  
L Barenghi ◽  
C Vergani ◽  
...  

2012 ◽  
Vol 32 (suppl_1) ◽  
Author(s):  
Benoit J Arsenault ◽  
Mathieu R Brodeur ◽  
David Rhainds ◽  
Anne-Elen Kernaleguen ◽  
Véronique Lavoie ◽  
...  

Background: Studies have shown that low HDL-cholesterol levels may be associated with the progression of aortic valvular calcium and aortic valvular stenosis (AVS), but whether patients with AVS have impaired cholesterol efflux capacities is unknown. Methods and results: We have measured four parameters of cholesterol efflux capacity in apolipoprotein B-depleted serum samples from 48 patients with (aortic jet velocity ≥2.5 m/s, mean age = 72 ± 7 years and 72.7% men) and 51 patients without AVS (aortic jet velocity ≤ 1.7 m/s, mean age 71 ± 7 years and 70.6% men). Cholesterol efflux capacity was measured using J774 macrophages with and without stimulation of ABCA1 expression by cAMP (non-stimulated efflux, total efflux and ABCA1-mediated efflux), and HepG2 hepatocytes to measure SR-BI-mediated efflux. Mean HDL-cholesterol and apolipoprotein A-I levels as well as efflux are shown in the table for patients with vs. without AVS. The Pearson correlation coefficient between HDL-cholesterol levels and SR-B1-dependent efflux was 0.39 (p=0.007) in patients with AVS and 0.68 (<0.0001) in controls (P-value for the difference between the correlation coefficients obtained with Fisher’s test = 0.04). Conclusions: This study provides evidence that serum from patients with AVS may have impaired cholesterol efflux capacities, especially through the SR-B1 pathway. Table. Mean HDL-cholesterol and apolipoprotein A-I levels as well as non-stimulated-, total-, ABCA1-, and SR-B1-dependent cholesterol efflux obtained from patients’ serum with vs. without AVS. Data is shown as mean ± SD. Differences between categories were assessed using a Student unpaired t-test.


1995 ◽  
Vol 96 (2) ◽  
pp. 177-182 ◽  
Author(s):  
Jerzy-Roch Nofer ◽  
Arnold Eckardstein ◽  
Heiko Wiebusch ◽  
Wei Weng ◽  
Harald Funke ◽  
...  

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