{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,5]],"date-time":"2026-04-05T00:08:22Z","timestamp":1775347702941,"version":"3.50.1"},"reference-count":37,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2013,2,9]],"date-time":"2013-02-09T00:00:00Z","timestamp":1360368000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Eur J Clin Investigation"],"published-print":{"date-parts":[[2013,4]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Objective<\/jats:title><jats:p>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 (<jats:styled-content style=\"fixed-case\">RCT<\/jats:styled-content>) mechanisms also provide protection against this disease. <jats:styled-content style=\"fixed-case\">RCT<\/jats:styled-content> is defined as the removal of cholesterol from peripheral macrophage foam cells, via high\u2010density lipoproteins (<jats:styled-content style=\"fixed-case\">HDL<\/jats:styled-content>), and cholesterol transportation to the liver for excretion. We have previously shown in a preliminary study that <jats:styled-content style=\"fixed-case\">HDL<\/jats:styled-content>, isolated from premenopausal women, enhanced macrophage cholesterol efflux compared to <jats:styled-content style=\"fixed-case\">HDL<\/jats:styled-content> derived from age\u2010matched male subjects.<\/jats:p><\/jats:sec><jats:sec><jats:title>Materials and methods<\/jats:title><jats:p>Here, we expanded this study by analysing a larger population of healthy volunteers and evaluated the capacity of <jats:styled-content style=\"fixed-case\">HDL<\/jats:styled-content> 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 <jats:styled-content style=\"fixed-case\">THP<\/jats:styled-content>\u20101 macrophages. <jats:styled-content style=\"fixed-case\">HDL<\/jats:styled-content> isolated from serum samples was incubated with [<jats:sup>3<\/jats:sup>H] cholesterol oleate\u2010loaded macrophages for 16\u00a0h, after which cholesterol efflux to <jats:styled-content style=\"fixed-case\">HDL<\/jats:styled-content> was determined.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>No significant differences in the efflux\u2010promoting ability of <jats:styled-content style=\"fixed-case\">HDL<\/jats:styled-content> existed among the three groups. Relevant plasma factors involved in further steps of <jats:styled-content style=\"fixed-case\">RCT<\/jats:styled-content>, such as cholesterol ester transfer protein (<jats:styled-content style=\"fixed-case\">CETP<\/jats:styled-content>), phospholipid transfer protein (<jats:styled-content style=\"fixed-case\">PLTP<\/jats:styled-content>) and lecithin:cholesterol acyltransferase (<jats:styled-content style=\"fixed-case\">LCAT<\/jats:styled-content>) activities were also analysed, but no differences were observed among the study groups.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>The results do not support a role for estradiol status or gender in modifying the initial step of <jats:styled-content style=\"fixed-case\">RCT<\/jats:styled-content> as a protective mechanism against cardiovascular disease.<\/jats:p><\/jats:sec>","DOI":"10.1111\/eci.12044","type":"journal-article","created":{"date-parts":[[2012,12,21]],"date-time":"2012-12-21T19:05:26Z","timestamp":1356116726000},"page":"317-323","source":"Crossref","is-referenced-by-count":29,"title":["The impact of gender and serum estradiol levels on <scp>HDL<\/scp>\u2010mediated reverse cholesterol transport"],"prefix":"10.1111","volume":"43","author":[{"given":"Robert M.","family":"Badeau","sequence":"first","affiliation":[{"name":"Turku PET Centre Turku University Central Hospital Turku Finland"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jari","family":"Metso","sequence":"additional","affiliation":[{"name":"National Institute for Health and Welfare Public Health Genomics Research Unit, Biomedicum Helsinki Finland"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Petri T.","family":"Kovanen","sequence":"additional","affiliation":[{"name":"Wihuri Research Institute Helsinki 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