A. Voneckardstein et al., PHOSPHOLIPID TRANSFER PROTEIN-MEDIATED CONVERSION OF HIGH-DENSITY-LIPOPROTEINS GENERATES BETA(1)-HDL, Biochimica et biophysica acta, L. Lipids and lipid metabolism, 1301(3), 1996, pp. 255-262
High density lipoproteins (HDL) subclasses can be differentiated by tw
o-dimensional non-denaturing polyacrylamide gradient gel electrophores
is (2D-PAGGE) and subsequent immunoblotting. The quantitatively minor
HDL-subclasses pre beta(1)-LpA-I and gamma-LpE are initial accepters o
f cell-derived cholesterol into the plasma compartment. In this study
we analysed the effect of phospholipid transfer protein (PLTP) on the
electrophoretic distribution of HDL-subclasses in plasma as well as th
e ability of plasma, pre beta(1)-LpA-I, and gamma-LpE to take up [H-3]
cholesterol from labeled fibroblasts. Pre beta(1)-LpA-I but not gamma-
LpE disappeared during a 16 hours incubation in the absence of PLTP. D
uring a one minute incubation pre beta(1)-LpA-I of pre-incubated plasm
a released 75% less [H-3]cholesterol from radiolabeled fibroblasts tha
n pre beta(1)-LpA-I of control plasma. Pre-incubation of plasma reduce
d the uptake of [H-3]cholesterol by gamma-LpE by 40%. Totally, the cho
lesterol efflux capacity of plasma decreased by 10% compared to the or
iginal sample. The amount of immunodetectable pre beta(1)-LpA-I increa
sed when plasma was incubated in the presence of PLTP while the amount
of immunodetectable gamma-LpE did not change. After one minute incuba
tion of PLTP-conditioned plasma with [H-3]cholesterol-labeled fibrobla
sts, the amount of radioactive cholesterol taken up by pre beta(1)-LpA
-I was twice as high as in control plasma whereas the amount of [H-3]c
holesterol taken up by gamma-LpE remained unchanged. As a net result,
treatment with PLTP increased the cholesterol efflux into total plasma
by 40%. Together with results of previous studies our data suggest th
at the conversion of alpha-LpA-I-3 into alpha-LpA-I-2 by PLTP generate
s pre beta(1)-LpA-I but not gamma-LpE. PLTP helps to enhance the uptak
e of cell-derived cholesterol by pre beta(1)-LpA-I and, thereby, the c
holesterol efflux capacity of normal plasma.