Deficiency of serum cholesteryl-ester transfer activity in patients with familial hyperalphalipoproteinaemia

Koizumi, Junji; Mabuchi, Hiroshi; Yoshimura, Atsushi; Michishita, Ichiro; Takeda, Masayoshi; Itoh, Hideaki; Sakai, Yasuyuki; Sakai, Takeshi; Ueda, Kosei; Takeda, Ryoyu

doi:10.1016/0021-9150(85)90064-4

Cited by 242 publications

(100 citation statements)

References 21 publications

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“…Sustained inhibition of CETP expression with antisense oligonucleotides increased plasma HDL-C and reduced atherosclerotic lesions in a rabbit model of atherosclerosis. 15 Transgenic mice 16 and rats 17 expressing CETP have decreased plasma concentrations of HDL-C. Human populations with reduced or absent CETP activity due to genetic mutations have markedly elevated plasma HDL-C. 6,18 Collectively, these data suggest that reducing CETP levels or activity could provide a benefit for individuals at risk of developing CHD.…”

Section: See Page 2029mentioning

confidence: 99%

Vaccine-Induced Antibodies Inhibit CETP Activity In Vivo and Reduce Aortic Lesions in a Rabbit Model of Atherosclerosis

Rittershaus

Miller

Thomas

et al. 2000

ATVB

294

152

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Abstract-Using a vaccine approach, we immunized New Zealand White rabbits with a peptide containing a region of cholesteryl ester transfer protein (CETP) known to be required for neutral lipid transfer function. These rabbits had significantly reduced plasma CETP activity and an altered lipoprotein profile. In a cholesterol-fed rabbit model of atherosclerosis, the fraction of plasma cholesterol in HDL was 42% higher and the fraction of plasma cholesterol in LDL was 24% lower in the CETP-vaccinated group than in the control-vaccinated group. Moreover, the percentage of the aorta surface exhibiting atherosclerotic lesion was 39.6% smaller in the CETP-vaccinated rabbits than in controls. The data reported here demonstrate that CETP activity can be reduced in vivo by vaccination with a peptide derived from CETP and support the concept that inhibition of CETP activity in vivo can be antiatherogenic. In addition, these studies suggest that vaccination against a self-antigen is a viable therapeutic strategy for disease management. (Arterioscler

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Section: See Page 2029mentioning

confidence: 99%

Vaccine-Induced Antibodies Inhibit CETP Activity In Vivo and Reduce Aortic Lesions in a Rabbit Model of Atherosclerosis

Rittershaus

Miller

Thomas

et al. 2000

ATVB

294

152

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“…CETP deficiency in human was firstly reported in Japanese hyperalphalipoproteinemia (HALP) [6]. Complete CETP deficiency presents extremely high HDL-cholesterol level and relatively low low density lipoprotein cholesterol (LDL-C) level [7].…”

Section: Introductionmentioning

confidence: 99%

Novel mutations of cholesteryl ester transfer protein (CETP) gene in Japanese hyperalphalipoproteinemic subjects

Ohtani

Inazu

Noji

et al. 2012

Clinica Chimica Acta

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Background: The half of hyperalphalipoproteinemia (HALP) in Japan is caused by CETP gene mutations. Other than two prevalent mutations (D442G and Intron 14 splicing donor site +1 G>A), some rare CETP mutations are found in Japanese HALP subjects.Methods: CETP gene analysis of genomic DNA from subjects was performed by restriction fragment length polymorphism (RFLP) and sequencing analysis. Mutations which were suspected to cause a splicing defect or a protein secretion defect were investigated in COS-1 cells transfected with a CETP minigene construct or a cDNA expression vector.Results: Each of three subjects was identified as a carrier of CETP gene mutation of a compound heterozygote of c.653_654delGGinsAAAC and Intron 14 splicing donor site +1 G>A, a heterozygote of c.658G>A or a homozygote of L261R. The c.658G>A mutation was located at the last nucleotide of exon 7, and it was confirmed to cause splicing abnormality revealed by the CETP minigene analysis. The L261R CETP was not secreted to conditioned media of the cells.Conclusions: Three novel CETP gene mutations are responsible for HALP by CETP deficiency. It is predicted that there are more rare CETP gene mutations in Japanese, and these multiple rare mutations alone or a combination with each of prevalent mutations responsible for mild-to-moderate or marked HALP, respectively.3

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“…1,2 Increased activity of plasma cholesteryl ester transfer protein (CETP), which facilitates the reverse cholesterol transport of cholesteryl ester from the HDL fraction to triglyceride (TG)-rich lipoproteins, is negatively related to the level of plasma HDL-cholesterol. CETP deficiencies, due to mutations in the CETP gene, which is located on chromosome 16q21, are associated with high levels of HDL-cholesterol, 3 and therefore might be related to longevity. Several studies report on the association between plasma HDL-cholesterol concentrations and the restriction fragment length polymorphism (RFLP) in intron 1 of the CETP gene.…”

Section: Introductionmentioning

confidence: 99%

TaqIB polymorphism in CETP gene: the influence on incidence of cardiovascular disease in statin-treated patients with familial hypercholesterolemia

Mohrschladt

Beer

Hofman³

et al. 2005

Eur J Hum Genet

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The effects of TaqI restriction fragment length polymorphism of the CETP gene on the occurrence of cardiovascular disease (CVD) events were investigated in patients with familial hypercholesterolemia (FH). A total of 300 FH patients, of which 116 (39%) had CVD at the start of the study, were treated with statins during a mean period of 8.5 years. The distribution of Taq1B genotypes was 31% B1B1, 49% B1B2, and 20% B2B2. No differences were found at baseline between the three genotypes, except for an association of the B1 allele with lower high-density lipoprotein (HDL)-cholesterol levels (P ¼ 0.003). All patients were put on statins within 6-8 weeks after the first visit; about 60% received simvastatin (20 -40 mg daily) and 40% either pravastatin (40 mg daily) or atorvastatin (20-40 mg daily). The different statin treatments were similar for all groups. The mean change of plasma HDL-cholesterol, low-density lipoproteincholesterol, and triglyceride concentration during statin therapy was similar for the three genotypes. During follow-up, new CVD events were recorded in 22 (37%) of the B2B2 patients (n ¼ 59) and in 67 (28%) of B1 allele carriers (n ¼ 241) (P ¼ 0.36). The relative risk for CVD events, after adjustment for age, gender, and CVD at intake, was 1.8 (CI: 1.1 -3.0) for B2B2 carriers compared to B1 allele carriers. The Taq1B polymorphism is a significant predictor of future CVD events in statin-treated patients with FH. In spite of similar improvement of the lipoprotein profile during statin therapy, our FH patients with the B2B2 genotype may have a higher CVD risk in comparison with the B1 allele carriers.

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Deficiency of serum cholesteryl-ester transfer activity in patients with familial hyperalphalipoproteinaemia

Cited by 242 publications

References 21 publications

Vaccine-Induced Antibodies Inhibit CETP Activity In Vivo and Reduce Aortic Lesions in a Rabbit Model of Atherosclerosis

Vaccine-Induced Antibodies Inhibit CETP Activity In Vivo and Reduce Aortic Lesions in a Rabbit Model of Atherosclerosis

Novel mutations of cholesteryl ester transfer protein (CETP) gene in Japanese hyperalphalipoproteinemic subjects

TaqIB polymorphism in CETP gene: the influence on incidence of cardiovascular disease in statin-treated patients with familial hypercholesterolemia

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