Interaction between high-density lipoprotein subpopulations in apo B-free and abetalipoproteinemic plasma.
Two populations of high-density lipoprotein (HDL) particles exist in human plasma. Both contain apolipoprotein (apo) A-I, but only one contains apo A-II: Lp(AI w AII) and Lp(AI w/o AII). To study the extent of interaction between these particles, apo B-free plasma prepared by the selective removal of apo B-containing lipoproteins (LpB) from the plasma of three normolipidemic (NL) subjects and whole plasma from two patients with abetalipoproteinemia (ABL) were incubated at 37 degrees C for 24 h. Apo B-free plasma samples were used to avoid lipid-exchange between HDL and LpB. Lp(AI w AII) and Lp(AI w/o AII) were isolated from each apo B-free plasma sample before and after incubation and their protein and lipid contents quantified. Before incubation, ABL plasma had reduced levels of Lp(AI w AII) and Lp(AI w/o AII), (40% and 70% of normals, respectively). Compared to the HDL of apo B-free NL plasma, ABL HDL had higher relative contents of free cholesterol, phospholipid and total lipid, and contained more particles with apparent hydrated Stokes diameter in the 9.2-17.0 nm region. These differences were particularly pronounced in particles without apo A-II. Despite their differences, the total cholesterol contents of Lp(AI w AII) increased, while that of Lp(AI w/o AII) decreased in all five plasma samples and the amount of apo A-I in Lp(AI w AII) increased by 6-8 mg/dl in four during the incubation. These compositional changes were accompanied by a relative reduction of particles in the 7.0-8.2 nm Stokes diameter size region and an increase of particles in the 9.2-11.2 nm region. These data are consistent with intravascular modulation between HDL particles with and without apo A-II. The observed increase in apo A-II-associated cholesterol and apo A-I, could involve either the transfer of cholesterol and apo A-I from particles without apo A-II to those with A-II, or the transfer of apo A-II from Lp(AI w AII) to Lp(AI w/o AII). The exact mechanism and direction of the transfer remain to be determined.
Cheung
M C
MC
Department of Medicine, University of Washington, Seattle 98103.
Wolf
A C
AC
Illingworth
D R
DR
D016632:Apolipoprotein A-I / Q000032:analysis; D016633:Apolipoprotein A-II / Q000032:analysis; D001055:Apolipoproteins B / Q000097:blood*; D002784:Cholesterol / Q000097:blood; D006801:Humans; D006995:Hypobetalipoproteinemias / Q000097:blood*; D050356:Lipid Metabolism; D008055:Lipids / Q000097:blood; D008075:Lipoproteins, HDL / Q000737:chemistry / Q000302:isolation & purification / Q000378:metabolism*; D010316:Particle Size; D010743:Phospholipids / Q000097:blood
D016632:Apolipoprotein A-I; D016633:Apolipoprotein A-II; D001055:Apolipoproteins B; D008055:Lipids; D008075:Lipoproteins, HDL; D010743:Phospholipids; D002784:Cholesterol