Pj. Pussinen et al., The role of plasma phospholipid transfer protein (PLTP) in HDL remodeling in acute-phase patients, BBA-MOL C B, 1533(2), 2001, pp. 153-163
Citations number
58
Categorie Soggetti
Biochemistry & Biophysics
Journal title
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR AND CELL BIOLOGY OF LIPIDS
During reverse cholesterol transport plasma phospholipid transfer protein (
PLTP) converts high density lipoprotein., (HDL3) into two new subpopulation
s, HDL2-like particles and pre-beta -HDL. The acute-phase response is accom
panied with dramatic changes in lipid metabolism including alterations in H
DL concentration, composition, and thereby its function as a substrate for
HDL remodeling proteins in circulation. To evaluate how acute-phase HDL (AP
-HDL) functions in PLTP-mediated HDL conversion, we collected plasma sample
s from patients with severe acute-phase response (n = 17), and from healthy
controls (n = 30). Subsequently, total HDL (1.063 < d < 1.21 g/ml) was iso
lated from patients and controls and incubated in the absence and presence
of purified PLTP. The results show that HDL isolated from the acute-phase p
atients is converted by PLTP in vitro in a corresponding manner as normal H
DL. In the combined population, C-reactive protein correlated significantly
with lecithin-cholesterol acyltransferase (LCAT) activity (r = -0.53), cho
lesterol ester transfer protein activity (r = -0.80), PLTP activity (r = 0.
44), and PLTP mass (r = -0.66). When compared to the controls, the patients
had 31% higher PLTP activity, but 52% lower PLTP mass leading to a 165% hi
gher PLTP specific activity in the patients. The present data indicate that
during the acute-phase response, plasma PUP activity and mass are strongly
affected by the lipoprotein distribution as well as lipid composition. We
suggest that the decrease of HDL during the acute phase is caused by reduce
d LCAT and increased PLTP activities both increasing the plasma levels of l
ipid-poor apoA-I particles. (C) 2001 Elsevier Science B.V. All rights reser
ved.