Aging affects high-density lipoprotein composition and function

被引:102
作者
Holzer, Michael [1 ]
Trieb, Markus [1 ]
Konya, Viktoria [1 ]
Wadsack, Christian [2 ]
Heinemann, Akos [1 ]
Marsche, Gunther [1 ]
机构
[1] Med Univ Graz, Inst Expt & Clin Pharmacol, Graz, Austria
[2] Med Univ Graz, Dept Obstet & Gynecol, Graz, Austria
来源
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR AND CELL BIOLOGY OF LIPIDS | 2013年 / 1831卷 / 09期
基金
奥地利科学基金会;
关键词
Proteome; Cardiovascular disease; Paraoxonase; Anti-oxidative activity; CHOLESTEROL EFFLUX CAPACITY; ALTERS HDL COMPOSITION; PHOSPHOLIPID TRANSFER PROTEIN; CORONARY-ARTERY-DISEASE; ANTIINFLAMMATORY PROPERTIES; COMPLEMENT ACTIVATION; LDL OXIDATION; IN-VIVO; RECEPTOR; ATHEROSCLEROSIS;
D O I
10.1016/j.bbalip.2013.06.004
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Most coronary deaths occur in patients older than 65 years. Age associated alterations in the composition and function of high-density lipoproteins (HDL) may contribute to cardiovascular mortality. The effect of advanced age on the composition and function of HDL is not well understood. HDL was isolated from healthy young and elderly subjects. HDL composition, cellular cholesterol efflux/uptake, anti-oxidant properties and paraoxonase activity were assessed. We observed a 3-fold increase of the acute phase protein serum amyloid A, an increased content of complement 0 and proteins involved in endopeptidase/protease inhibition in HDL of elderly subjects, whereas levels of apolipoprotein E were significantly decreased. HDL from elderly subjects contained less cholesterol but increased sphingomyelin. Most importantly, HDL from elderly subjects showed defective antioxidant properties, lower paraoxonase 1 activity and was more rapidly taken up by macrophages, whereas cholesterol efflux capability was not altered. These findings suggest that aging alters HDL composition, resulting in functional impairment that may contribute to the onset/progression of cardiovascular disease. (C) 2013 The Authors. Published by Elsevier B.V. All rights reserved.
引用
收藏
页码:1442 / 1448
页数:7
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