Lipids in Health and Disease,
Journal Year:
2007,
Volume and Issue:
6(1), P. 24 - 24
Published: Jan. 1, 2007
CD36,
an
88
kDa
membrane
glycoprotein,
is
found
in
several
cell
types
and
it
has
been
characterized
to
have
two
hydrophobic
domains
at
their
N-
C-termini
which
are
essential
for
protein
folding
targeting.
In
this
study,
we
first
tagged
the
green
fluorescent
(GFP)
both
of
huCD36
investigated
cellular
expression
influences
on
lipoprotein
plasmodium
falciparium
parasitized
erythrocytes
(pRBC)
binding.
Our
work
revealed
that
proteins
expressed
normally
irrespective
GFP
tag
presence
either
or
C-termini.
However,
recombinant
showed
discrepancy
uptake
surface-binding
OxLDL
but
they
did
not
affect
pRBC
These
results
suggested
interaction
between
oxLDL
CD36
could
be
blocked
using
may
useful
potential
control
trafficking
modified
lipoproteins
into
monocytes
leading
atherogenesis.
Diabetic Medicine,
Journal Year:
2010,
Volume and Issue:
28(1), P. 61 - 72
Published: Sept. 27, 2010
Diabet.
Med.
28,
61–72
(2011)
Abstract
Aims
To
determine
fasting
and
postprandial
metabolism
of
apolipoprotein
B48
(apoB48)
remnant
lipoproteins
in
subjects
with
Type
1
diabetes
the
relationship
to
progressive
cardiovascular
disease,
investigate
impact
lipoprotein
cholesterol
accumulation
associated
arterial
wall
biglycan
using
a
rodent
model
diabetes.
Methods
Normolipidaemic
(
n
=
9)
long‐standing
(and
advanced
disease)
seven
healthy
control
were
studied.
Fasting
apoB48
concentration
was
determined
following
sequential
meal
challenge.
A
streptozotocin‐induced
used
ex
vivo
retention
fluorescent‐conjugated
remnants.
Binding
human
recombinant
assessed
vitro
.
Results
significantly
higher
plasma
remnants
observed
patients
compared
subjects.
Patients
exhibited
greater
total
area
under
curve
(AUC)
an
increased
incremental
AUC
second
The
sevenfold
rats
relative
controls.
Remnants
shown
bind
significant
affinity
further
2.3‐fold
binding
capacity
glycated
biglycan.
colocalize
both
matrix
proteins
model.
Conclusion
Impaired
enhanced
proteoglycans
appears
contribute
deposition
Our
findings
support
hypothesis
that
impaired
may
accelerated
progression
atherosclerosis
hyperglycaemic
insulin‐deficient
state.
Nutrition Metabolism and Cardiovascular Diseases,
Journal Year:
2010,
Volume and Issue:
21(11), P. 871 - 878
Published: Aug. 3, 2010
Atherosclerosis
is
known
to
be
an
inflammatory
disease
and
there
increasing
evidence
that
chylomicron
remnants
(CMR),
the
lipoproteins
which
carry
dietary
fats
in
blood,
cause
macrophage
foam
cell
formation
inflammation.
In
early
atherosclerosis
frequency
of
activated
monocytes
peripheral
circulation
increased,
clearance
CMR
from
blood
may
delayed,
however,
whether
contribute
directly
monocyte
activation
subsequent
egress
into
arterial
wall
has
not
been
established.
Here,
contribution
pro-inflammatory
pathways
was
assessed
using
vitro
model.Primary
human
CMR-like
particles
(CRLP)
were
used
measure
several
endpoints
activation.
Treatment
with
CRLP
caused
rapid
prolonged
generation
reactive
oxygen
species
by
monocytes.
The
chemokines
MCP-1
IL-8
secreted
nanogram
quantities
cells
absence
CRLP.
secretion
transiently
increased
after
treatment,
maintained
presence
pharmacological
inhibitors
production.
contrast,
exposure
significantly
reduced
secretion.
Chemotaxis
towards
pre-exposed
reversed
addition
exogenous
MCP-1.Our
findings
indicate
activate
augment
their
migration
reducing
cellular
expression.
Our
data
support
current
hypothesis
milieu
atherosclerosis,
suggest
this
reflect
direct
interaction
circulating
Frontiers in Cardiovascular Medicine,
Journal Year:
2019,
Volume and Issue:
6
Published: June 25, 2019
Cardiovascular
diseases
(CVDs)
and
chronic
obstructive
pulmonary
disease
(COPD)
are
the
two
leading
causes
of
mortality
morbidity
worldwide
that
coexist
frequently.
Most
recent
studies
have
concluded
patients
with
CVD
or
risk
factors
for
more
likely
to
major
adverse
cardiovascular
events
(MACEs)
after
an
acute
exacerbation
COPD,
severe
COPD
higher
than
those
less
COPD.
The
MACEs
in
is
determined
by
complex
interactions
between
genetics,
behavioral,
metabolic
environmental
factors.
To
date,
there
no
guidelines
regarding
prevention,
screening,
management
modifiable
context
exacerbations,
insufficient
control
It
not
clear
whether
tight
individual
(e.g.,
smoking
cessation)
composite
will
reduce
deaths
from
cardiac
events.
A
deeper
insight
may
improve
strategies
reduction
Key
words:
Chronic
disease,
diseases,
events,
FEBS Letters,
Journal Year:
2005,
Volume and Issue:
579(29), P. 6537 - 6542
Published: Nov. 2, 2005
We
investigated
the
interaction
of
oxidized
low
density
lipoprotein
(OxLDL)
with
ATP‐binding
cassette
A1
(ABCA1)
pathway
in
J774
macrophages.
Cellular
efflux
to
apolipoprotein
AI
(apo‐AI)
OxLDL‐derived
cholesterol
was
lower
than
derived
from
acetylated
(AcLDL).
ABCA1
upregulation
by
8‐(4‐chlorophenylthio)adenosine
3′:5′‐cyclic
monophosphate
(cpt‐cAMP)
or
22
(R)‐hydroxycholesterol
(22‐OH)
and
9‐
cis
retinoic
acid
(9cRA)
increased
apo‐AI
cellular
sterols
AcLDL,
but
not
those
OxLDL.
OxLDL,
induced
protein
content
activity
J774.
However,
OxLDL
did
influence
cpt‐cAMP
22‐OH/9cRA.
conclude
that
released
cells
are
available
neither
as
substrate
nor
modulator
ABCA1.
Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids,
Journal Year:
2007,
Volume and Issue:
1771(7), P. 901 - 910
Published: May 4, 2007
The
influence
of
the
oxidative
state
chylomicron
remnants
(CMR)
on
mechanisms
their
uptake
and
induction
lipid
accumulation
by
macrophages
derived
from
human
monocyte
cell
line,
THP-1,
during
foam
formation
was
investigated
using
chylomicron-remnant-like
particles
(CRLPs)
at
3
different
levels
oxidation.
CRLPs
varied
exposure
to
CuSO(4)
(oxCRLPs)
or
incorporation
antioxidant,
probucol
(pCRLPs)
into
particles.
oxCRLPs
caused
significantly
less
triacylglycerol
in
than
CRLPs,
rate
lower,
while
pCRLPs
more
were
taken
up
faster.
Uptake
all
types
inhibited
a
similar
extent
when
entry
via
low
density
lipoprotein
(LDL)
receptor
related
protein
(80-90%),
LDL
(-30-40%),
CD36
(-40%)
phagocytosis
(-35-40%)
blocked
lactoferrin,
excess
LDL,
anti-CD36
cytochalasin
D,
respectively,
but
blocking
scavenger
receptors-A
-B1
poly
inosinic
acid
HDL
had
no
effect.
These
findings
show
that
oxidation
lowers
macrophages.
However,
does
not
change
main
pathways
internalisation
THP-1
macrophages,
which
occur
mainly
LRP
with
some
contribution
LDLr,
have
only
minor
role,
regardless
Thus,
effects
CMR
contrast
sharply
those
this
may
be
important
role
dietary
oxidized
lipids
antioxidants
modulating
atherosclerosis.
Lipids,
Journal Year:
2011,
Volume and Issue:
46(4), P. 371 - 380
Published: Jan. 31, 2011
Abstract
Macrophages
in
arterial
walls
accumulate
lipids
leading
to
the
development
of
atherosclerotic
plaques.
However,
mechanisms
underlying
macrophage
lipid
accumulation
and
foam
cell
formation
are
often
studied
without
accounting
for
risk
factors
such
as
dyslipidemia.
We
investigated
effect
varying
concentrations
triglyceride
(TG)
within
physiological
range
on
fatty
acid
(FA)
expression
cholesterol
efflux
proteins.
Human
monocytes
were
cultured
media
supplemented
with
10%
sera
containing
low
(0.7
mmol/L)
high
(1.4
TG.
The
resulting
macrophages
harvested
after
10
days
analysis
FA
content
composition
genes
involved
metabolism.
Exposure
higher
TG
lower
HDL
increased
content.
exposed
had
total
compared
controls
(876
μg/mg
protein
vs.
652
protein)
greater
proportions
C16:0,
C18:1
C18:2.
Macrophage
both
ABCA1
ABCG1
proteins
reduced
when
present
media.
Expression
scavenger
receptor
CD36,
lipoprotein
uptake,
was
also
downregulated
Culturing
conditions
versus
influenced
composition,
levels
regulatory
Replicating
vitro
dyslipidemia
encountered
vivo
may
provide
an
informative
model
investigation
atherogenesis.