A1 Vertaisarvioitu alkuperäisartikkeli tieteellisessä lehdessä
The impact of gender and serum estradiol levels on HDL-mediated reverse cholesterol transport
Tekijät: Badeau RM, Metso J, Kovanen PT, Lee-Rueckert M, Tikkanen MJ, Jauhiainen M
Kustantaja: WILEY-BLACKWELL
Kustannuspaikka: HOBOKEN; 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
Julkaisuvuosi: 2013
Journal: European Journal of Clinical Investigation
Tietokannassa oleva lehden nimi: European journal of clinical investigation
Lehden akronyymi: Eur.J.Clin.Invest.
Numero sarjassa: 4
Vuosikerta: 43
Numero: 4
Aloitussivu: 317
Lopetussivu: 323
Sivujen määrä: 7
ISSN: 0014-2972
DOI: https://doi.org/10.1111/eci.12044
Tiivistelmä
Objective Premenopausal women have a lower incidence of cardiovascular disease compared to men of the same age. Endogenous oestrogens, especially estradiol, presumably protect against atherosclerosis by a variety of mechanisms. Reverse cholesterol transport (RCT) mechanisms also provide protection against this disease. RCT is defined as the removal of cholesterol from peripheral macrophage foam cells, via high-density lipoproteins (HDL), and cholesterol transportation to the liver for excretion. We have previously shown in a preliminary study that HDL, isolated from premenopausal women, enhanced macrophage cholesterol efflux compared to HDL derived from age-matched male subjects. Materials and methods Here, we expanded this study by analysing a larger population of healthy volunteers and evaluated the capacity of HDL derived from women with high or low serum E2 concentrations, mainly representing premenopausal and postmenopausal women, respectively, or men (each group consisting of 30 subjects) to facilitate cholesterol removal from human THP-1 macrophages. HDL isolated from serum samples was incubated with [3H] cholesterol oleate-loaded macrophages for 16h, after which cholesterol efflux to HDL was determined. Results No significant differences in the efflux-promoting ability of HDL existed among the three groups. Relevant plasma factors involved in further steps of RCT, such as cholesterol ester transfer protein (CETP), phospholipid transfer protein (PLTP) and lecithin:cholesterol acyltransferase (LCAT) activities were also analysed, but no differences were observed among the study groups. Conclusion The results do not support a role for estradiol status or gender in modifying the initial step of RCT as a protective mechanism against cardiovascular disease.
Objective Premenopausal women have a lower incidence of cardiovascular disease compared to men of the same age. Endogenous oestrogens, especially estradiol, presumably protect against atherosclerosis by a variety of mechanisms. Reverse cholesterol transport (RCT) mechanisms also provide protection against this disease. RCT is defined as the removal of cholesterol from peripheral macrophage foam cells, via high-density lipoproteins (HDL), and cholesterol transportation to the liver for excretion. We have previously shown in a preliminary study that HDL, isolated from premenopausal women, enhanced macrophage cholesterol efflux compared to HDL derived from age-matched male subjects. Materials and methods Here, we expanded this study by analysing a larger population of healthy volunteers and evaluated the capacity of HDL derived from women with high or low serum E2 concentrations, mainly representing premenopausal and postmenopausal women, respectively, or men (each group consisting of 30 subjects) to facilitate cholesterol removal from human THP-1 macrophages. HDL isolated from serum samples was incubated with [3H] cholesterol oleate-loaded macrophages for 16h, after which cholesterol efflux to HDL was determined. Results No significant differences in the efflux-promoting ability of HDL existed among the three groups. Relevant plasma factors involved in further steps of RCT, such as cholesterol ester transfer protein (CETP), phospholipid transfer protein (PLTP) and lecithin:cholesterol acyltransferase (LCAT) activities were also analysed, but no differences were observed among the study groups. Conclusion The results do not support a role for estradiol status or gender in modifying the initial step of RCT as a protective mechanism against cardiovascular disease.
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