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Apolipoprotein E protects cultured pericytes and astrocytes from D-Abeta(1-40)-mediated cell death.
[hereditary cerebral hemorrhage with amyloidosis]
Cerebral
amyloid
angiopathy
(
CAA
)
is
a
common
pathological
finding
in
Alzheimer
's
disease
and
hereditary
cerebral
hemorrhage
with
amyloidosis
of
the
Dutch
type
;
in
this
latter
condition
it
is
caused
by
deposition
of
mutated
amyloid
beta
protein
(
Abeta
Glu
22
G
ln
;
D-Abeta
(
1
-
40
)
)
.
Previously
,
we
found
a
dependence
of
the
Abeta-mediated
toxicity
and
apolipoprotein
E
(
apoE
)
production
by
cultured
pericytes
on
apoE
genotype
.
Given
their
close
association
with
the
cerebrovascular
wall
both
astrocytes
and
pericytes
may
be
involved
in
CAA
development
,
a
process
that
includes
Abeta
deposition
and
clearance
and
that
may
be
affected
by
interaction
with
locally
produced
apolipoprotein
E
(
apoE
)
.
Although
astrocytes
are
regarded
as
the
major
source
of
apolipoprotein
E
(
apoE
)
in
the
brain
,
also
pericytes
produce
apoE
.
In
this
study
we
compared
the
apoE
production
capacity
,
the
effects
of
apoE
on
D-Abeta
(
1
-
40
)
internalization
,
D-Abeta
(
1
-
40
)
cell
surface
accumulation
and
the
vulnerability
for
D-Abeta
(
1
-
40
)
-
induced
toxicity
of
either
cell
type
in
order
to
quantify
the
relative
contributions
of
astrocytes
and
pericytes
in
the
various
processes
that
contribute
to
CAA
formation
.
Strikingly
,
cultured
astrocytes
produced
only
3
-
10
%
of
the
apoE
amounts
produced
by
pericytes
.
Furthermore
,
pericytes
with
the
apoE
epsilon
4
allele
produced
three
times
less
apoE
and
were
more
vulnerable
to
D-Abeta
(
1
-
40
)
treatment
than
pericytes
without
an
epsilon
4
allele
.
Such
relations
were
not
observed
with
astrocytes
in
vitro
.
Both
pericytes
and
astrocytes
,
however
,
were
protected
from
Abeta-induced
cytotoxicity
by
high
levels
of
pericyte-derived
apoE
,
but
not
recombinant
apoE
.
In
addition
,
pericyte-derived
apoE
dose-dependently
decreased
both
internalization
of
Abeta
and
Abeta
accumulation
at
the
cell
surface
in
either
cell
type
.
The
present
data
suggest
that
apoE
produced
by
pericytes
,
rather
than
astrocyte-produced
apoE
,
modulates
Abeta
cytotoxicity
and
Abeta
removal
near
the
vasculature
in
the
brain
.
Furthermore
,
since
apoE
production
in
pericytes
is
genotype
dependent
,
this
may
contribute
to
the
apoE
genotype-dependent
development
of
CAA
in
vivo
.
Diseases
Validation
Diseases presenting
"common pathological finding"
symptom
hereditary cerebral hemorrhage with amyloidosis
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