Project Details
Abstract
The
endoplasmic
reticulum
(ER)
is
the
cellular
site
for
Ca2+
storage
and
for
synthesis,
folding,
and
maturation
of
most
secreted
and
transmembrane
proteins.
ER
stress
occurs
when
there
is
an
imbalance
between
the
cellular
demand
for
ER
function
and
ER
capacity.
There
is
increasing
evidence
suggesting
that
ER
stress
is
associated
with
a
range
of
diseases,
including
ischemia/reperfusion
injury
and
pregnancy
complications
such
as
intrauterine
growth
restriction
(IUGR).
Our
previous
work
shows
that
hypoxia-‐reoxygenation
(HR)
is
a
possible
mechanism
for
placental
oxidative
stress
in
preeclampsia
and
IUGR.
Here
we
will
apply
this
model
to
induce
ER
stress
and
investigate
possible
mechanisms
for
ER
stress-‐related
apoptosis
in
cytotrophoblasts.
Cytotrophoblast
cells
will
be
obtained
from
normal
term
placentas
and
used
to
study
the
changes
of
Bcl-‐2
family
proteins
and
Ca2+
homeostasis
in
ER
and
activation
of
the
Ire1/TRAF2/Ask1
signaling
pathway.
We
will
also
compare
the
levels
of
ER
stress
between
placentas
from
pregnancy
complicated
by
IUGR
and
those
from
normal
pregnancy.
The
results
will
extend
our
understanding
of
the
role
of
ER
stress
in
trophoblast
cell
death.
Project IDs
Project ID:PC10101-2055
External Project ID:NSC100-2314-B182A-082-MY3
External Project ID:NSC100-2314-B182A-082-MY3
Status | Finished |
---|---|
Effective start/end date | 01/08/12 → 31/07/13 |
Keywords
- placenta
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