Characterization of phospholipids in pre-alpha HDL: selective phospholipid efflux with apolipoprotein A-I.
نویسندگان
چکیده
Previously, we have shown that lipid-free apoA-I, when incubated with fibroblasts, will produce lipoproteins of pre-alpha mobility (Asztalos, B. F., et al. 1997. Arterioscler. Thromb. Vasc. Biol. 17: 1630-1636). In order to understand the nature of these pre-alpha particles, we further characterized their lipid content. The pre-alpha particles are high density lipoproteins, having a median density of 1.08 g/ml. They have a surface charge of -18.45 mV. The phospholipid composition of these particles showed that they have 4% each of phosphatidyl ethanolamine and inositol; 69% phosphatidyl choline and 18% sphingomyelin. This phospholipid composition is different from those of plasma HDL (81% phosphatidyl choline, 13% sphingomyelin), plasma membrane on the fibroblasts, and whole fibroblast phospholipid. To demonstrate that the pre-alpha mobility resides in the lipids, lipids from pre-alpha lipoproteins were reconstituted with lipid-free apoA-I. The resultant particles retained their pre-alpha mobility. We conclude that apoA-I may react with specific regions of plasma membrane to acquire this unusual lipid composition and that pre-alpha mobility is caused in part by the unusual phospholipid composition.
منابع مشابه
Characterization of phospholipids in pre- a HDL: selective phospholipid efflux with apolipoprotein A-I
Previously, we have shown that lipid-free apoA-I, when incubated with fibroblasts, will produce lipoproteins of prea mobility (Asztalos, B. F., et al. 1997. Arterioscler. Thromb. Vasc. Biol. 17: 1630–1636). In order to understand the nature of these prea particles, we further characterized their lipid content. The prea particles are high density lipoproteins, having a median density of 1.08 g/m...
متن کاملPlasma and fibroblasts of Tangier disease patients are disturbed in transferring phospholipids onto apolipoprotein A-I.
Plasmas of patients with Tangier disease (TD) lack lipid-rich alpha-HDL which, in normal plasma, constitutes the majority of high density lipoprotein (HDL). Residual amounts of apolipoprotein (apo)A-I in TD plasma occur as lipid-poor or even lipid-free prebeta-HDL. By contrast to normal plasma, TD plasma does not convert prebeta-HDL into alpha-HDL. Moreover, fibroblasts of TD patients were foun...
متن کاملBehavior of human apolipoprotein A-I: phospholipid and apoHDL:phospholipid complexes in vitro and after injection into rabbits.
Apolipoprotein A-I was purified from human high density lipoprotein and complexed with polyunsaturated phosphatidylcholine (PC) in deoxycholate (Lipostabil); the bile salt was removed subsequently by dialysis. The behavior of the resultant apoA-I/PC complexes was compared with that of Lipostabil in vitro and after injection into rabbits. In vivo apoA-I/PC complexes had the density of HDL throug...
متن کاملCharacterization and properties of pre beta-HDL particles formed by ABCA1-mediated cellular lipid efflux to apoA-I.
The contribution of ABCA1-mediated efflux of cellular phospholipid (PL) and cholesterol to human apolipoprotein A-I (apoA-I) to the formation of pre beta 1-HDL (or lipid-poor apoA-I) is not well defined. To explore this issue, we characterized the nascent HDL particles formed when lipid-free apoA-I was incubated with fibroblasts in which expression of the ABCA1 was upregulated. After a 2 h incu...
متن کاملDefective removal of cellular cholesterol and phospholipids by apolipoprotein A-I in Tangier Disease.
Tangier disease is a rare genetic disorder characterized by extremely low plasma levels of HDL and apo A-I, deposition of cholesteryl esters in tissues, and a high prevalence of cardiovascular disease. We examined the possibility that HDL apolipoprotein-mediated removal of cellular lipids may be defective in Tangier disease. With fibroblasts from normal subjects, purified apo A-I cleared cells ...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
عنوان ژورنال:
- Journal of lipid research
دوره 39 8 شماره
صفحات -
تاریخ انتشار 1998