© 1995 American Heart Association, Inc.
Articles |
High-Density Lipoproteins Inhibit Cytokine-Induced Expression of Endothelial Cell Adhesion Molecules
From the Hanson Center for Cancer Research, Department of Human Immunology, Department of Lipid Research (G.W.C., J.R.G., M.A.V.), the Cardiovascular Investigation Unit, Royal Adelaide Hospital (K.-A.R.), and the University of Adelaide, Department of Medicine, Royal Adelaide Hospital (P.J.B.), Adelaide, Australia.
Correspondence to Gillian Cockerill, Hanson Center for Cancer Research, Department of Human Immunology, IMVS, PO Box 14, Rundle Mall, Adelaide 5000, South Australia. E-mail gcockeri@immuno.imvs.sa.gov.au.
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Abstract |
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Abstract While an elevated plasma concentration of HDLs is protective against the development of atherosclerosis and ensuing coronary heart disease (CHD), the mechanism of this protection is unknown. One early cellular event in atherogenesis is the adhesion of mononuclear leukocytes to the endothelium. This event is mediated principally by vascular cell adhesion molecule-1 (VCAM-1) but also involves other molecules, such as intercellular adhesion molecule-1 (ICAM-1) and E-selectin. We have investigated the effect of isolated plasma HDLs and reconstituted HDLs on the expression of these molecules by endothelial cells. We show that physiological concentrations of HDLs inhibit tumor necrosis factor-
(TNF-) or interleukin-1 (IL-1) induction of
these leukocyte adhesion molecules in a concentration-dependent
manner. Steady state mRNA levels of TNF-–induced VCAM-1 and
E-selectin are significantly reduced by
physiological concentrations of HDLs. At an HDL
concentration of 1 mg/mL apolipoprotein A-I, the protein expressions of
VCAM-1, ICAM-1, and E-selectin were inhibited by 89.6±0.4% (mean±SD,
n=4), 64.8±1.0%, and 79.2±0.4%, respectively. In contrast, HDLs
have no effect on the expression of platelet
endothelial cell adhesion molecule (PECAM) or on the
expression of the p55 and p75 subunits of the TNF- receptor. HDLs
were effective when added from 16 hours before to 5 minutes after
cytokine stimulation. HDLs had no effect on
TNF-–induced expression of ICAM-1 by human foreskin
fibroblasts, suggesting that the effect is cell-type restricted.
This study provides the first evidence that HDLs may protect
against CHD by inhibiting the expression of adhesion molecules,
which are required for the interaction between leukocytes and the
endothelium.
Key Words: inflammation • coronary heart disease • VCAM-1 • E-selectin
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Introduction |
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Atherosclerotic CHD is still one of the major causes of death in the western world.1 Epidemiological studies have shown a strong inverse correlation between the concentration of plasma HDLs and the incidence of CHD.2 3 Direct evidence of a protective effect of HDLs has come from the studies of transgenic mice, in which high levels of expression of human apoA-I, the major apolipoprotein in HDLs, increased the HDL concentrations and gave protection against diet-induced atherosclerosis.4 It is not yet known whether the protection relates to the involvement of HDLs in reverse cholesterol transport or whether HDLs protect against CHD by a mechanism unrelated to their lipid transport function.
An early event in atherogenesis is the adhesion of monocytes to
the endothelium via adhesion molecules such as VCAM-1,
ICAM-1, and E-selectin, all of which are rapidly synthesized in
response to cytokines. VCAM-1 (CD106) is a member of the
immunoglobulin-like superfamily and is primarily involved in the
adhesion of mononuclear leukocytes to the endothelium.
VCAM-1 is rapidly induced by the inflammatory cytokines IL-1
and TNF-, and its induction is sustained for 48 to 72 hours. ICAM-1
(CD54) is expressed on many cell types and is involved in both monocyte
and lymphocyte adhesion to activated
endothelium. E-selectin (CD62E) is an
endothelial-specific adhesion molecule important in
the adhesion of polymorphonuclear leukocytes, monocytes, and
lymphocytes to cytokine-treated HUVECs.5 6 7 8 9 10 11 12 13 14 It
has also been shown to be important in capturing leukocytes from the
axial stream to roll along the
endothelium.15
There is considerable evidence for the involvement of adhesion molecules in the development of early atherosclerotic lesions16 and in mature atherosclerotic plaques.17 The expression of VCAM-1 is coincident with early foam cell lesions in hypercholesterolemic rabbits.16 Variable and low levels of E-selectin and VCAM-1 have been detected in the arterial endothelium over plaques.17 18 VCAM-1 has also been observed in areas of neovascularization and inflammatory infiltrates at the base of plaques, suggesting that intimal neovascularization may be an important site of inflammatory cell recruitment into advanced coronary lesions.19 ICAM-120 and P-selectin, another member of the selectin family also involved in the rolling of leukocytes, have also been shown to be expressed on the endothelium overlaying atheromatous plaques, suggesting that leukocyte adhesion and recruitment into the plaque may be mediated through a synergy between the selectins and members of the immunoglobulin-like superfamily of adhesion molecules.21
The concept of the critical role of adhesion molecules in atherogenesis has been strengthened by reports showing that LDLs,22 especially if minimally oxidized,23 increase monocyte adhesion to endothelial cells. Furthermore, it has been shown that lysophosphatidylcholine, a major component of oxidatively modified LDLs, induces expression of VCAM-1 and ICAM-1.24 25 These observations suggest that LDLs promote atherogenesis at least in part by this mechanism. In this study we test the hypothesis that HDLs may have a direct effect on the endothelium by inhibiting the induced expression of adhesion molecules.
We show that physiological levels of native and reconstituted HDLs inhibit the induction of adhesion molecules on endothelial cells. These observations strongly point to a specific role for HDLs in preventing the adhesion-dependent early events in atherogenesis and in preventing the progression of atheromata by a similar mechanism. Therefore, this study demonstrates a function of HDL beyond those previously described.
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Methods |
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Cell Culture
HUVECs were isolated as described previously.26 All cells were cultured on gelatin-coated culture flasks in medium M199 with Earle's salts (Cytosystems) supplemented with 20% fetal calf serum (GIBCO), 20 mmol/L HEPES, 2 mmol/L glutamine, 1 mmol/L sodium pyruvate, nonessential amino acids, penicillin, streptomycin, 50 µg/mL endothelial growth supplement (Collaborative Research), and 50 µg/mL heparin (Sigma). Confluent HUVECs were incubated for 16 hours in varying concentrations of HDLs; then TNF-
or IL-1 (100 U/mL) was added to the culture medium and incubated for an
additional 4 hours, at which time the cell-surface expression of
VCAM-1, E-selectin, and ICAM-1 were measured by flow cytometry. In the
case of TNF- receptor and PECAM, cells were incubated for 20 hours
in HDLs but were not cytokine stimulated before assay of their
expression by flow cytometry.
Flow Cytometry Analysis
Cells were harvested by trypsinization, and then washed in PBS.
Levels of cell-surface expression of proteins were measured by
incubation of the cell suspension in 50 µL of primary antibody for 30
minutes at 4°C. Cells were then washed in FACS wash (PBS containing
0.02% azide and 5% newborn calf serum) at 4°C, resuspended in 50
µL of FACS wash containing the appropriate FITC-conjugated secondary
antibody, and incubated at 4°C for an additional 30 minutes. After
another wash, the cell pellet was resuspended in FACS fixative (PBS
containing 2% glucose, 0.02% azide, and 2.5% formaldehyde), and
expression of cell-surface molecules was measured as
fluorescence intensity by use of a Coulter Epics Profile
II flow cytometer. Each sample counted 1x104 cells.
Controls for each assay included the absence of primary antibody and
the incubation of the cells with an isotype-matched, nonrelevant
antibody.
Antibodies Used
Mouse monoclonal antibody to VCAM-1 (10C9) and mouse monoclonal
antibody to E-selectin (49-1B11) were generated in our laboratory and
characterized by their ability to bind to VCAM-1– and
E-selectin–transfected Chinese hamster ovary cells, respectively.
The TNF receptor antibodies for the p75 subunit (utr-1) and the p55
subunit (htr-9) were a gift from Dr Brockhaus (Roche). The rabbit
polyclonal antibody against PECAM was a gift from Dr Micheal Berndt
(Baker Institute).
Northern Blot Analysis
Total RNA was prepared as described by Chomczynski and
Sacchi.27 Equal aliquots of total RNA (10 µg) were
electrophoresed in a 1% formaldehyde gel and transferred to nylon
membrane (Hybond N, Amersham). RNA was fixed in a UV strata-linker
(Stragagene). The blots were prehybridized according to Church and
Gilbert28 and hybridized with 10 ng/mL
32P-labeled cDNA probes. After washing, the blots were
exposed on Kodak XAR5 film (Eastman Kodak). Relative amounts of RNA per
lane were normalized to the ethidium bromide–stained ribosomal
RNAs.
Isolation of HDLs
Blood samples from normal healthy donors under 40 years of age
were collected in EDTA-Na2 (final concentration, 1 mg/mL).
Plasma was separated by centrifugation at 4°C. HDLs
were isolated by sequential ultracentrifugation in
the 1.07- to 1.21-g/mL density range, as described
elsewhere.29 Resulting preparations of HDLs were dialyzed
against four changes of PBS before filter sterilization with 0.2-mm
acrodiscs (Gelman Sciences).
The concentrations of apoA-I and apoB in the preparations of HDLs were determined immunoturbidimetrically on a Cobas-Fara centrifugal analyzer (Roche Diagnostic). The apoA-I and apoB antibodies and standards were obtained from Boehringer Mannheim. HDL particle size distribution was evaluated by electrophoresis on a 3% to 35% nondenaturing gradient gel according to manufacturer's recommendations (Pharmacia LKB Biotechnology). All preparations of HDLs contained two main populations: one with particles of Stokes' diameter 10.45 nm (HDL2b) and one with particles of diameter 8.6 nm (HDL3a). There was no evidence of contamination by particles in the size range of LDLs, and no apoB was detected in the HDL preparations.
Preparation of Reconstituted HDL Particles
Discoidal reconstituted A-I HDL was prepared by the cholate
dialysis method from egg-yolk phosphatidylcholine, unesterified
cholesterol, and apoA-I.30 ApoA-I was prepared
from human plasma, as described elsewhere.31 Egg-yolk
phosphatidylcholine, unesterified cholesterol, and sodium
cholate were obtained from Sigma and used without further purification.
Particle size was measured by nondenaturing gradient gel
electrophoresis, and concentration of apoA-I was measured
immunoturbidimetrically, as described above.
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Results |
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HDLs Inhibit Both TNF-
–Induced and IL-1–Induced VCAM-1
Expression on Endothelial CellsBoth IL-1 and TNF-
have been shown to induce the expression of
VCAM-1 on endothelial cells.32 To test the
hypothesis that HDLs inhibit cytokine-induced
expression of VCAM-1, confluent HUVEC monolayers were incubated for 16
hours in the presence of HDLs at an apoA-I concentration of 1 mg/mL
before the addition of IL-1 or TNF-. After an additional 4 hours of
incubation, cell-surface expression of VCAM-1 was determined by
flow cytometry. Fig 1
shows that both IL-1 (A) and
TNF- (B) induce the expression of VCAM-1 on HUVECs (solid line),
and that HDLs (1 mg/mL apoA-I, dashed line) inhibit the expression of
VCAM-1 in both IL-1–stimulated (A) and TNF-–stimulated (B)
HUVECs. In similarly designed experiments, preincubation of HUVECs
with native LDL or oxidized LDL did not alter the level of
cytokine-induced expression of adhesion molecules (data
not shown). Consistent with the findings of Khan et
al,33 we showed no induction of
endothelial cell adhesion molecule expression by native
or oxidized LDL per se (data not shown).
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Concentration-Dependent Effects of HDLs on TNF-–Induced
Expression of Adhesion Molecules
Cytokine stimulation of HUVECs also leads to the induced
expression of ICAM-1 and E-selectin, as well as VCAM-1.32
To compare the effects of HDLs on VCAM-1 with those on ICAM-1 and
E-selectin expression, we incubated endothelial
monolayers for 16 hours with a range of concentrations of HDLs before
the addition of TNF-. HDLs inhibited the TNF-–induced
expression of VCAM-1 in a concentration-dependent manner (Fig 2). At a concentration of 1 mg/mL apoA-I, HDLs reduce
the expression of VCAM-1 by 89.6±0.4% (mean±SD, n=4).
TNF-–induced expression of ICAM-1 and E-selectin was also
inhibited in a concentration-dependent manner, with inhibition of
64.8±1.0% and 79.2±0.4%, respectively, at an apoA-I concentration
of 1 mg/mL. To exclude the possibility that the decrease in
cytokine-induced expression of adhesion molecules was
an artifact resulting from residual HDLs sterically hindering access of
the antibodies to their respective antigens, flow cytometry was
performed in the presence and absence of exogenous HDLs. Monolayers of
HUVECs were stimulated with TNF- (100 U/mL for 4 hours). After
removal of the cell monolayer by trypsinization, the cells were
resuspended in the respective primary antibodies in the presence of
HDLs over a range of concentrations. The Table shows
that HDL concentrations of up to 1.0 mg/mL apoA-I did not change the
detectability of cell-surface molecules.
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HDLs Reduce Steady State mRNA Levels of VCAM-1 and
E-Selectin
The effects of HDLs on steady state levels of mRNA of VCAM-1 and
E-selectin in endothelial cells were investigated.
Confluent endothelial cells were incubated (1) for 20
hours with no addition, (2) for 16 hours with no addition followed by 4
hours in the presence of TNF- (100 U/mL), and (3) for 16 hours with
HDLs at a physiological concentration (1 mg/mL
apoA-I) before adding TNF- for an additional 4 hours of incubation.
After completion of the incubations, total RNA was extracted, and the
levels of mRNA specific for VCAM-1 and E-selectin were measured by
Northern blot analysis with cDNA probes (Fig 3).
In the uninduced samples there was no detectable message for either
VCAM-1 or E-selectin. In the samples induced by TNF- in the absence
of HDL, the level of message for both adhesion molecules was
substantial. The levels of message for both VCAM-1 and E-selectin were
markedly reduced by HDLs.
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HDLs Have No Effect on Expression of PECAM and TNF
Receptor
PECAM is constitutively expressed on endothelial
cells.34 To investigate the possibility that incubation of
endothelial cells with HDLs had a nonspecific effect on
the expression of all molecules, we examined the effect of HDLs on the
expression of PECAM. There was no change in PECAM expression after a
20-hour incubation of HUVEC monolayers with a range of concentrations
of HDLs (Fig 4).
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The p55 and p75 subunits of the TNF- receptor are also
constitutively expressed on endothelial
cells.35 We examined whether incubation of HUVECs with
HDLs could result in a reduction in cell-surface expression of
TNF- receptor. We incubated confluent HUVECs with HDLs (1 mg/mL
apoA-I) for 20 hours. TNF- receptor expression was then assayed by
flow cytometry. Fig 5 shows flow cytometric profiles of
HUVECs stained with antibodies against the p55 (dashed line) and p75
(dotted line) subunits of the TNF- receptor in the presence versus
the absence of HDLs. The presence of HDLs had no effect on the levels
of expression of these molecules.
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Time Course of Inhibition of VCAM-1 Expression by
HDLs
To establish the time dependence of the inhibitory
effect of HDLs on HUVECs, we examined the level of VCAM-1 expression 4
hours after TNF- treatment in cells to which HDLs (1 mg/mL apoA-I)
were added from 16 hours before to 4 hours after TNF-. Fig 6 shows that the inhibitory effect of HDLs
does not require preincubation, since significant inhibition
(86.4±0.6%) is obtained when HDLs (1 mg/mL apoA-I) are added at the
same time or even 5 minutes after the TNF-. However, when added 1 or
more hours after TNF- activation, the level of VCAM-1 expression is
comparable with the control cultures to which HDLs have not been added
(NA). When cell cultures were incubated for 16 hours with HDLs followed
by two washes in PBS, which removes >95% of the HDL (as determined by
measuring the recovered HDL according to the method described in
"Methods"), maximal inhibition of expression of
TNF-–induced VCAM-1 expression was observed (R).
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Since the inhibition of cytokine-induced VCAM-1
expression could be sustained when HDLs were removed before TNF-
stimulation, we investigated the kinetics of this acquired inhibition.
HDLs (1 mg/mL apoA-I) were added over a range of times to confluent
monolayers of HUVECs before being removed from the cultures by two
washes in PBS. Fresh medium containing TNF- was then added, and the
VCAM-1 expression was determined by flow cytometry 4 hours later. Fig 7 shows that the acquisition of inhibition was time
dependent, with 50% maximal inhibition requiring 
60 minutes of
incubation. With 10 minutes of preincubation with HDLs, no significant
difference in VCAM-1 expression is observed. After 30 minutes and 1
hour of preincubation, VCAM-1 expression was suppressed by 42.3±1.31%
and 56.5±0.6%, respectively. In cultures in which HDLs have been
preincubated for 2 hours, the level of TNF-–induced expression
of VCAM-1 was inhibited by 88.4±0.76%.
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HDLs Do Not Inhibit TNF-–Induced Induction of ICAM-1 in
Fibroblasts
ICAM-1 is expressed and regulated on fibroblasts. We examined the
ability of HDLs to inhibit the TNF-–induced expression of this
molecule on fibroblasts. Fig 8 shows that after a 4-hour
stimulation with TNF- (100 U/mL), ICAM-1 expression was
significantly (P<.005) induced from a basal level of
20.46±0.43 to 60.06±11.4 mean fluorescence intensity. When
incubated with HDLs (1 mg/mL apoA-I), the level of TNF-–induced
expression of ICAM-1 was not significantly altered (66.46±12.3).
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Reconstituted HDLs Inhibit the TNF--Induced Expression of
VCAM-1
To exclude the possibility that the inhibiting effects of plasma
HDLs were mediated by contaminating plasma components that
co-isolated with the HDLs, we investigated the effects of
reconstituted HDLs. Reconstituted discoidal HDLs containing purified
apoA-I as their sole protein, egg-derived phosphatidylcholine as
their sole phospholipid, and unesterified
cholesterol30 were incubated with HUVEC
monolayers before the addition of TNF-. We found that these
reconstituted HDLs inhibit the expression of VCAM-1 in a
concentration-dependent manner comparable with that of plasma HDLs
(Fig 9).
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Discussion |
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Our studies show an effect of HDLs on endothelial cells that is consistent with the proposition that HDLs have a direct inhibitory effect on one of the earliest events in atherogenesis. Their ability to inhibit cytokine-induced cell-surface expression of adhesion molecules raises the possibility that HDLs may inhibit atherogenesis at an early stage by preventing monocyte adhesion to the endothelium. The inhibitory effects of HDLs may also influence the progression of atheromata by altering the expression of adhesion molecules shown to be important in trafficking T lymphocytes to these lesions.
HDLs have been shown to have other functions unrelated to their role in
plasma cholesterol transport; these include acting as an
antioxidant,36 acting as a mitogen,37 and
having the ability to bind
lipopolysaccharide.38 A mitogenic
effect of HDLs on endothelial cells may protect against
vascular disease by maintaining an intact endothelium.
Finally, the binding of lipopolysaccharide to HDLs protects
against septic shock by rendering the toxin inaccessible to its
receptor (CD14)39 on the monocyte/macrophage, thus
preventing the subsequent release of cytokines, such as
TNF-, IL-1, and IL-6.40 Our current findings that
physiological concentrations of HDLs are able to
significantly inhibit the cytokine activation of adhesion
molecules on the endothelial cell suggest that HDLs may
also contribute to the protective effects of an acute inflammatory
response.
Experiments were conducted to exclude the possibility that the effects
of HDLs on the adhesion protein expression had a trivial explanation.
The possibility of artifact as a result of HDLs inhibiting the
detection of cell-surface proteins was excluded because we found no
interference of detection in the flow cytometry assay. Our results also
show that it is unlikely that HDLs are preventing access to the
cytokine receptor or are affecting the level of receptor
expression on the endothelial cell. We demonstrate no
difference in the ability to detect TNF-receptor subunit levels on
endothelial cells after 20 hours of incubation in HDLs.
It is also unlikely that HDLs are restricting availability of the
cytokine by binding it, as we show that removal of HDLs after a
2-hour preincubation followed by TNF- stimulation resulted in
maximal inhibition of VCAM-1 expression. Provided
endothelial cells had undergone a 2-hour incubation
with HDLs before cytokine stimulation, HDLs were not required
during the cytokine stimulation to achieve maximal inhibition.
The possibility that the inhibition of adhesion molecule expression may
be due to cytotoxic effects was excluded by the observation that cell
viability, as determined by the standard dye exclusion method and
plating efficiency of the cultures, remained >95% after a 20-hour
incubation in the presence of HDLs (1 mg/mL apoA-I). In addition,
confluent cultures maintained a healthy "cobblestone" morphology
in the presence of HDLs (data not shown), further suggesting that the
general metabolic state of the cell cultures was not
compromised. Inhibition was not donor specific and is highly
reproducible, as evidenced by the fact that all the experiments
reported have been completed on more than 20 donors of HUVECs with
different batches of HDLs.
In addition, all the above experiments with TNF- have been performed
and identical results obtained with the spontaneously transformed HUVEC
line C11STH,41 demonstrating that this cell line is an
appropriate model for future studies. In contrast to these results with
endothelial cells, the cytokine induction of
ICAM-1 on fibroblasts was unaffected by the presence of HDLs,
suggesting that the inhibitory effect of HDLs is restricted
to certain cell types.
We show that the addition of HDLs to endothelial cell
cultures at the same time or 5 minutes after the addition of TNF-
can inhibit cytokine-induced expression of adhesion
molecules. However, when HDLs were added to the cultures 1 hour after
TNF-, they were no longer able to inhibit the
cytokine-induced VCAM-1 expression, suggesting that
HDLs are operating to inhibit an early cell-signaling response to
the cytokine. TNF- has many overlapping actions with IL-1,
which has led to a suggestion of shared signal transduction mechanisms.
We show a qualitative similarity in the ability of HDLs to suppress
IL-1–induced or TNF-–induced adhesion molecule expression,
indicating that the mechanism of action is not receptor specific but
may be through a common signaling pathway.
It is noteworthy that HDLs inhibit the expression of all the adhesion proteins shown to support monocyte adhesion. Although there are other cytokines that also inhibit adhesion protein expression, these operate only on some proteins. Transforming growth factor-ß, for example, suppresses E-selectin but not VCAM-1 expression,42 and IL-4 increases VCAM-1 while decreasing E-selectin.43 Thus, HDLs appear unique in the breadth of their actions. Demonstration that the selectins and the immunoglobulin-like class of adhesion molecules may synergize to enable the recruitment and adhesion of leukocytes into the plaques is important in understanding the development of the atheroma.20 21 We demonstrate that HDLs are able to reduce the protein and mRNA levels of both classes of molecules; in this capacity they may be able to prevent the progression of existing atherosclerotic lesions. This suggestion is consistent with studies in which regression of atherosclerotic lesions occurs when animals are infused with HDLs.44
The demonstration that reconstituted HDLs that contain only apoA-I are able to mimic the effects of native HDL is very important because it suggests that the most protective apolipoprotein has a function ascribable to the whole plasma HDL. In addition, it makes it less likely that unidentified molecules copurified along with native HDL particles, rather than known components of HDL, are responsible for these effects. Clarification of the mechanism by which HDLs inhibit the expression of adhesion molecules and elucidation of the HDL subpopulations that are responsible may ultimately lead to the development of novel strategies for the prevention and treatment of atherosclerosis.
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Selected Abbreviations and Acronyms |
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Acknowledgments |
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This work was supported by funding from the National Health and Medical Council of Australia, the National Heart Foundation, and the Royal Adelaide Hospital Research Fund. We thank Neil Hime and Leanne Noack for technical assistance and Dr Peter Cockerill for many helpful discussions and critical reading of the manuscript. cDNAs for VCAM-1 and E-selectin were gifts from Brian Seed and Tucker Collins, respectively. We thank the staff of the delivery wards of Queen Victoria Hospital and Burnside War Memorial Hospital for collecting umbilical cords.
Received July 10, 1995; accepted August 18, 1995.
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P. Holvoet, K. Peeters, S. Lund-Katz, A. Mertens, P. Verhamme, R. Quarck, D. Stengel, M. Lox, E. Deridder, H. Bernar, et al. Arg123-Tyr166 Domain of Human ApoA-I Is Critical for HDL-Mediated Inhibition of Macrophage Homing and Early Atherosclerosis in Mice Arterioscler Thromb Vasc Biol, December 1, 2001; 21(12): 1977 - 1983. [Abstract] [Full Text] [PDF]
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J. X. Rong, J. Li, E. D. Reis, R. P. Choudhury, H. M. Dansky, V. I. Elmalem, J. T. Fallon, J. L. Breslow, and E. A. Fisher Elevating High-Density Lipoprotein Cholesterol in Apolipoprotein E-Deficient Mice Remodels Advanced Atherosclerotic Lesions by Decreasing Macrophage and Increasing Smooth Muscle Cell Content Circulation, November 13, 2001; 104(20): 2447 - 2452. [Abstract] [Full Text] [PDF]
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P. K. Shah, S. Kaul, J. Nilsson, and B. Cercek Exploiting the Vascular Protective Effects of High-Density Lipoprotein and Its Apolipoproteins: An Idea Whose Time for Testing Is Coming, Part I Circulation, November 6, 2001; 104(19): 2376 - 2383. [Full Text] [PDF]
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A. S. Major, D. E. Dove, H. Ishiguro, Y. R. Su, A. M. Brown, L. Liu, K. J. Carter, M. F. Linton, and S. Fazio Increased Cholesterol Efflux in Apolipoprotein AI (ApoAI)-Producing Macrophages as a Mechanism for Reduced Atherosclerosis in ApoAI(-/-) Mice Arterioscler Thromb Vasc Biol, November 1, 2001; 21(11): 1790 - 1795. [Abstract] [Full Text] [PDF]
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B. J. O'Connell and J. Genest Jr High-Density Lipoproteins and Endothelial Function Circulation, October 16, 2001; 104(16): 1978 - 1983. [Abstract] [Full Text] [PDF]
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G. W. COCKERILL, M. C. MCDONALD, H. MOTA-FILIPE, S. CUZZOCREA, N. E. MILLER, and C. THIEMERMANN High density lipoproteins reduce organ injury and organ dysfunction in a rat model of hemorrhagic shock FASEB J, September 1, 2001; 15(11): 1941 - 1952. [Abstract] [Full Text] [PDF]
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G. W. Cockerill, T. Y. Huehns, A. Weerasinghe, C. Stocker, P. G. Lerch, N. E. Miller, and D. O. Haskard Elevation of Plasma High-Density Lipoprotein Concentration Reduces Interleukin-1-Induced Expression of E-Selectin in an In Vivo Model of Acute Inflammation Circulation, January 2, 2001; 103(1): 108 - 112. [Abstract] [Full Text] [PDF]
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D. Sviridov, L. E. Pyle, M. Jauhiainen, C. Ehnholm, and N. H. Fidge Deletion of the propeptide of apolipoprotein A-I reduces protein expression but stimulates effective conversion of pre{beta}-high density lipoprotein to {alpha}-high density lipoprotein J. Lipid Res., November 1, 2000; 41(11): 1872 - 1882. [Abstract] [Full Text]
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G. THEILMEIER, B. DE GEEST, P. P. VAN VELDHOVEN, D. STENGEL, C. MICHIELS, M. LOX, M. LANDELOOS, M. J. CHAPMAN, E. NINIO, D. COLLEN, et al. HDL-associated PAF-AH reduces endothelial adhesiveness in apoE-/- mice FASEB J, October 1, 2000; 14(13): 2032 - 2039. [Abstract] [Full Text]
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P. W. Baker, K.-A. Rye, J. R. Gamble, M. A. Vadas, and P. J. Barter Phospholipid composition of reconstituted high density lipoproteins influences their ability to inhibit endothelial cell adhesion molecule expression J. Lipid Res., August 1, 2000; 41(8): 1261 - 1267. [Abstract] [Full Text]
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K. J. Williams, R. Scalia, K. D. Mazany, W. V. Rodrigueza, and A. M. Lefer Rapid Restoration of Normal Endothelial Functions in Genetically Hyperlipidemic Mice by a Synthetic Mediator of Reverse Lipid Transport Arterioscler Thromb Vasc Biol, April 1, 2000; 20(4): 1033 - 1039. [Abstract] [Full Text] [PDF]
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B. Foger, M. Chase, M. J. Amar, B. L. Vaisman, R. D. Shamburek, B. Paigen, J. Fruchart-Najib, J. A. Paiz, C. A. Koch, R. F. Hoyt, et al. Cholesteryl Ester Transfer Protein Corrects Dysfunctional High Density Lipoproteins and Reduces Aortic Atherosclerosis in Lecithin Cholesterol Acyltransferase Transgenic Mice J. Biol. Chem., December 24, 1999; 274(52): 36912 - 36920. [Abstract] [Full Text] [PDF]
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P. Xia, M. A. Vadas, K.-A. Rye, P. J. Barter, and J. R. Gamble High Density Lipoproteins (HDL) Interrupt the Sphingosine Kinase Signaling Pathway. A POSSIBLE MECHANISM FOR PROTECTION AGAINST ATHEROSCLEROSIS BY HDL J. Biol. Chem., November 12, 1999; 274(46): 33143 - 33147. [Abstract] [Full Text] [PDF]
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K. K. Koh, A. Blum, L. Hathaway, R. Mincemoyer, G. Csako, M. A. Waclawiw, J. A. Panza, and R. O. Cannon III Vascular Effects of Estrogen and Vitamin E Therapies in Postmenopausal Women Circulation, November 2, 1999; 100(18): 1851 - 1857. [Abstract] [Full Text] [PDF]
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K. Saku, B. Zhang, K. Shirai, S. Jimi, K. Yoshinaga, and K. Arakawa Hyperinsulinemic hypoalphalipoproteinemia as a new indicator for coronary heart disease J. Am. Coll. Cardiol., November 1, 1999; 34(5): 1443 - 1451. [Abstract] [Full Text] [PDF]
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R. K. Tangirala, K. Tsukamoto, S. H. Chun, D. Usher, E. Pure, and D. J. Rader Regression of Atherosclerosis Induced by Liver-Directed Gene Transfer of Apolipoprotein A-I in Mice Circulation, October 26, 1999; 100(17): 1816 - 1822. [Abstract] [Full Text] [PDF]
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L. Lindstedt, J. Saarinen, N. Kalkkinen, H. Welgus, and P. T. Kovanen Matrix Metalloproteinases-3, -7, and -12, but Not -9, Reduce High Density Lipoprotein-induced Cholesterol Efflux from Human Macrophage Foam Cells by Truncation of the Carboxyl Terminus of Apolipoprotein A-I. PARALLEL LOSSES OF PRE-beta PARTICLES AND THE HIGH AFFINITY COMPONENT OF EFFLUX J. Biol. Chem., August 6, 1999; 274(32): 22627 - 22634. [Abstract] [Full Text] [PDF]
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H. M. Dansky, S. A. Charlton, J. L. Sikes, S. C. Heath, R. Simantov, L. F. Levin, P. Shu, K. J. Moore, J. L. Breslow, and J. D. Smith Genetic Background Determines the Extent of Atherosclerosis in ApoE-Deficient Mice Arterioscler Thromb Vasc Biol, August 1, 1999; 19(8): 1960 - 1968. [Abstract] [Full Text] [PDF]
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L. E. P. Rohde, C. H. Hennekens, and P. M. Ridker Cross-Sectional Study of Soluble Intercellular Adhesion Molecule-1 and Cardiovascular Risk Factors in Apparently Healthy Men Arterioscler Thromb Vasc Biol, July 1, 1999; 19(7): 1595 - 1599. [Abstract] [Full Text] [PDF]
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J. A. McCrohon, W. Jessup, D. J. Handelsman, and D. S. Celermajer Androgen Exposure Increases Human Monocyte Adhesion to Vascular Endothelium and Endothelial Cell Expression of Vascular Cell Adhesion Molecule-1 Circulation, May 4, 1999; 99(17): 2317 - 2322. [Abstract] [Full Text] [PDF]
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G. W. Cockerill, J. Saklatvala, S. H. Ridley, H. Yarwood, N. E. Miller, B. Oral, S. Nithyanathan, G. Taylor, and D. O. Haskard High-Density Lipoproteins Differentially Modulate Cytokine-Induced Expression of E-Selectin and Cyclooxygenase-2 Arterioscler Thromb Vasc Biol, April 1, 1999; 19(4): 910 - 917. [Abstract] [Full Text] [PDF]
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N. H. Fidge High density lipoprotein receptors, binding proteins, and ligands J. Lipid Res., February 1, 1999; 40(2): 187 - 201. [Abstract] [Full Text]
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P. W. Baker, K.-A. Rye, J. R. Gamble, M. A. Vadas, and P. J. Barter Ability of reconstituted high density lipoproteins to inhibit cytokine-induced expression of vascular cell adhesion molecule-1 in human umbilical vein endothelial cells J. Lipid Res., February 1, 1999; 40(2): 345 - 353. [Abstract] [Full Text]
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K. Saku, B. Zhang, T. Ohta, and K. Arakawa Quantity and function of high density lipoprotein as an indicator of coronary atherosclerosis J. Am. Coll. Cardiol., February 1, 1999; 33(2): 436 - 443. [Abstract] [Full Text] [PDF]
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K. K. Koh, C. Cardillo, M. N. Bui, L. Hathaway, G. Csako, M. A. Waclawiw, J. A. Panza, and R. O. Cannon III Vascular Effects of Estrogen and Cholesterol-Lowering Therapies in Hypercholesterolemic Postmenopausal Women Circulation, January 26, 1999; 99(3): 354 - 360. [Abstract] [Full Text] [PDF]
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P. Benoit, F. Emmanuel, J. M. Caillaud, L. Bassinet, G. Castro, P. Gallix, J. C. Fruchart, D. Branellec, P. Denefle, and N. Duverger Somatic Gene Transfer of Human ApoA-I Inhibits Atherosclerosis Progression in Mouse Models Circulation, January 12, 1999; 99(1): 105 - 110. [Abstract] [Full Text] [PDF]
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L. E. Rohde, R. T. Lee, J. Rivero, M. Jamacochian, L. H. Arroyo, W. Briggs, N. Rifai, P. Libby, M. A. Creager, and P. M. Ridker Circulating Cell Adhesion Molecules Are Correlated With Ultrasound-Based Assessment of Carotid Atherosclerosis Arterioscler Thromb Vasc Biol, November 1, 1998; 18(11): 1765 - 1770. [Abstract] [Full Text] [PDF]
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D. T. Ashby, K.-A. Rye, M. A. Clay, M. A. Vadas, J. R. Gamble, and P. J. Barter Factors Influencing the Ability of HDL to Inhibit Expression of Vascular Cell Adhesion Molecule-1 in Endothelial Cells Arterioscler Thromb Vasc Biol, September 1, 1998; 18(9): 1450 - 1455. [Abstract] [Full Text] [PDF]
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Y. Abe, B. El-Masri, K. T. Kimball, H. Pownall, C. F. Reilly, K. Osmundsen, C. W. Smith, and C. M. Ballantyne Soluble Cell Adhesion Molecules in Hypertriglyceridemia and Potential Significance on Monocyte Adhesion Arterioscler Thromb Vasc Biol, May 1, 1998; 18(5): 723 - 731. [Abstract] [Full Text] [PDF]
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R. Batal, M. Tremblay, L. Krimbou, O. Mamer, J. Davignon, J. Genest Jr, and J. S. Cohn Familial HDL Deficiency Characterized by Hypercatabolism of Mature ApoA-I but Not ProApoA-I Arterioscler Thromb Vasc Biol, April 1, 1998; 18(4): 655 - 664. [Abstract] [Full Text] [PDF]
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S.-J. Hwang, C. M. Ballantyne, A. R. Sharrett, L. C. Smith, C. E. Davis, A. M. Gotto Jr, and E. Boerwinkle Circulating Adhesion Molecules VCAM-1, ICAM-1, and E-selectin in Carotid Atherosclerosis and Incident Coronary Heart Disease Cases : The Atherosclerosis Risk In Communities (ARIC) Study Circulation, December 16, 1997; 96(12): 4219 - 4225. [Abstract] [Full Text]
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A. Matsumoto, A. Mitchell, H. Kurata, L. Pyle, K. Kondo, H. Itakura, and N. Fidge Cloning and Characterization of HB2, a Candidate High Density Lipoprotein Receptor. SEQUENCE HOMOLOGY WITH MEMBERS OF THE IMMUNOGLOBULIN SUPERFAMILY OF MEMBRANE PROTEINS J. Biol. Chem., July 4, 1997; 272(27): 16778 - 16782. [Abstract] [Full Text] [PDF]
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