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Aberrant cell cycle reentry in human and experimental inclusion body myositis and polymyositis.
[inclusion body myositis]
Inclusion
body
myositis
(
IBM
)
,
a
degenerative
and
inflammatory
disorder
of
skeletal
muscle
,
and
Alzheimer
's
disease
share
protein
derangements
and
attrition
of
postmitotic
cells
.
Overexpression
of
cyclins
and
proliferating
cell
nuclear
antigen
(
PCNA
)
and
evidence
for
DNA
replication
is
reported
in
Alzheimer
's
disease
brain
,
possibly
contributing
to
neuronal
death
.
It
is
unknown
whether
aberrant
cell
cycle
reentry
also
occurs
in
IBM
.
We
examined
cell
cycle
markers
in
IBM
compared
with
normal
control
,
polymyositis
(
PM
)
and
non-
inflammatory
dystrophy
sample
sets
.
Next
,
we
tested
for
evidence
of
reentry
and
DNA
synthesis
in
C
2
C
12
myotubes
induced
to
express
β-amyloid
(
Aβ
42
)
.
We
observed
increased
levels
of
Ki-
67
,
PCNA
and
cyclins
E
/
D
1
in
IBM
compared
with
normals
and
non-
inflammatory
conditions
.
Interestingly
,
PM
samples
displayed
similar
increases
.
Satellite
cell
markers
did
not
correlate
with
Ki-
67
-
affected
myofiber
nuclei
.
DNA
synthesis
and
cell
cycle
markers
were
induced
in
A
β-bearing
myotubes
.
Cell
cycle
marker
and
cyclin
protein
expressions
were
also
induced
in
an
experimental
allergic
myositis
-like
model
of
PM
in
mice
.
Levels
of
p
21
(
Cip
1
/
WAF
1
)
,
a
cyclin-dependent
kinase
inhibitor
,
were
decreased
in
affected
myotubes
.
However
,
overexpression
of
p
21
did
not
rescue
cells
from
Aβ-induced
toxicity
.
This
is
the
first
report
of
cell
cycle
reentry
in
human
myositis
.
The
absence
of
rescue
and
evidence
for
reentry
in
separate
models
of
myodegeneration
and
inflammation
suggest
that
new
DNA
synthesis
may
be
a
reactive
response
to
either
or
both
stressors
.
Diseases
Validation
Diseases presenting
"absence of rescue"
symptom
inclusion body myositis
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