High-density lipoprotein-associated sphingosine-1-phosphate activity in heterozygous familial hypercholesterolaemia.

Details

Serval ID
serval:BIB_8C88517BE8D3
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
High-density lipoprotein-associated sphingosine-1-phosphate activity in heterozygous familial hypercholesterolaemia.
Journal
European journal of clinical investigation
Author(s)
Frias M.A., Thomas A., Brulhart-Meynet M.C., Kövamees O., Pernow J., Eriksson M., Angelin B., James R.W., Brinck J.W.
ISSN
1365-2362 (Electronic)
ISSN-L
0014-2972
Publication state
Published
Issued date
01/2017
Peer-reviewed
Oui
Volume
47
Number
1
Pages
38-43
Language
english
Notes
Publication types: Journal Article
Publication Status: ppublish
Abstract
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.
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.
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.
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.

Pubmed
Web of science
Create date
25/11/2016 14:35
Last modification date
20/08/2019 15:50
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