Journal article
High-density lipoprotein-associated sphingosine-1-phosphate activity in heterozygous familial hypercholesterolaemia.
- Frias MA Department of internal medicine specialities, Medical Faculty, Geneva University, Geneva, Switzerland.
- Thomas A Unit of Toxicology, University Centre of Legal Medicine, Lausanne-Geneva, Switzerland.
- Brulhart-Meynet MC Department of internal medicine specialities, Medical Faculty, Geneva University, Geneva, Switzerland.
- Kövamees O Division of Cardiology, Department of Medicine, Karolinska Institutet at Karolinska University Hospital Solna, Stockholm, Sweden.
- Pernow J Division of Cardiology, Department of Medicine, Karolinska Institutet at Karolinska University Hospital Solna, Stockholm, Sweden.
- Eriksson M Metabolism Unit, Department of Endocrinology, Metabolism and Diabetes, Centre for Innovative Medicine, Karolinska Institutet, Stockholm, Sweden.
- Angelin B Metabolism Unit, Department of Endocrinology, Metabolism and Diabetes, Centre for Innovative Medicine, Karolinska Institutet, Stockholm, Sweden.
- James RW Department of internal medicine specialities, Medical Faculty, Geneva University, Geneva, Switzerland.
- Brinck JW Department of internal medicine specialities, Medical Faculty, Geneva University, Geneva, Switzerland.
- 2016-11-19
Published in:
- European journal of clinical investigation. - 2017
Apolipoprotein M
cardiomyocyte
high-density lipoprotein
oxidative stress
sphingosine-1-phosphate
Adult
Animals
Apolipoprotein A-I
Case-Control Studies
Cells, Cultured
Cholesterol, HDL
Chromatography, Liquid
Female
Heterozygote
Humans
Hydroxymethylglutaryl-CoA Reductase Inhibitors
Hyperlipoproteinemia Type II
In Vitro Techniques
Lipoproteins, HDL
Lysophospholipids
Male
Middle Aged
Myocytes, Cardiac
Oxidative Stress
Rats
Sphingosine
Tandem Mass Spectrometry
Young Adult
English
BACKGROUND
Patients with heterozygous familial hypercholesterolaemia (FH) suffer from high plasma cholesterol and an environment of increased oxidative stress. We examined its potential effects on high-density lipoprotein (HDL)-associated sphingosine-1-phosphate (S1P) content (HDL-S1P) and HDL-mediated protection against oxidative stress, both with and without statin treatment.
MATERIALS AND METHODS
In a case-control study, HDL was isolated from 12 FH patients with and without statin treatment and from 12 healthy controls. The HDL-S1P content and the capacity of HDL to protect cardiomyocytes against oxidative stress in vitro were measured.
RESULTS
HDL-associated S1P was significantly correlated with cell protection, but not with HDL-cholesterol or apolipoprotein AI. The latter did not correlate with HDL-mediated cell protection. Neither the HDL-S1P content nor HDL protective capacity differed between nontreated FH patients and controls. The relative amounts of apolipoprotein AI and apolipoprotein M were similar between controls and FH patients. Statin treatment had no effect on any of these measures.
CONCLUSIONS
The FH environment is not detrimental to HDL-S1P content or HDL-S1P-mediated cell protection. Statin treatment does not modulate HDL function in this regard.
Patients with heterozygous familial hypercholesterolaemia (FH) suffer from high plasma cholesterol and an environment of increased oxidative stress. We examined its potential effects on high-density lipoprotein (HDL)-associated sphingosine-1-phosphate (S1P) content (HDL-S1P) and HDL-mediated protection against oxidative stress, both with and without statin treatment.
MATERIALS AND METHODS
In a case-control study, HDL was isolated from 12 FH patients with and without statin treatment and from 12 healthy controls. The HDL-S1P content and the capacity of HDL to protect cardiomyocytes against oxidative stress in vitro were measured.
RESULTS
HDL-associated S1P was significantly correlated with cell protection, but not with HDL-cholesterol or apolipoprotein AI. The latter did not correlate with HDL-mediated cell protection. Neither the HDL-S1P content nor HDL protective capacity differed between nontreated FH patients and controls. The relative amounts of apolipoprotein AI and apolipoprotein M were similar between controls and FH patients. Statin treatment had no effect on any of these measures.
CONCLUSIONS
The FH environment is not detrimental to HDL-S1P content or HDL-S1P-mediated cell protection. Statin treatment does not modulate HDL function in this regard.
- Language
-
- English
- Open access status
- closed
- Identifiers
-
- DOI 10.1111/eci.12699
- PMID 27861771
- Persistent URL
- https://sonar.ch/global/documents/77919
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