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Estrogen deficiency reversibly induces telomere shortening in mouse granulosa cells and ovarian aging in vivo.
[aromatase deficiency]
Estrogen
is
implicated
as
playing
an
important
role
in
aging
and
tumorigenesis
of
estrogen
responsive
tissues
;
however
the
mechanisms
underlying
the
mitogenic
actions
of
estrogen
are
not
fully
understood
.
Here
we
report
that
estrogen
deficiency
in
mice
caused
by
targeted
disruption
of
the
aromatase
gene
results
in
a
significant
inhibition
of
telomerase
maintenance
of
telomeres
in
mouse
ovaries
in
a
tissue-
specific
manner
.
The
inhibition
entails
a
significant
shortening
of
telomeres
and
compromised
proliferation
in
the
follicular
granulosa
cell
compartment
of
ovary
.
Gene
expression
analysis
showed
decreased
levels
of
proto-oncogene
c-
Myc
and
the
telomerase
catalytic
subunit
,
telomerase
reverse
transcriptase
(
TERT
)
,
in
response
to
estrogen
deficiency
.
Estrogen
replacement
therapy
led
to
increases
in
TERT
gene
expression
,
telomerase
activity
,
telomere
length
and
ovarian
tissue
growth
,
thereby
reinstating
ovary
development
to
normal
in
four
weeks
.
Our
data
demonstrate
for
the
first
time
that
telomere
maintenance
is
the
primary
mechanism
mediating
the
mitogenic
effect
of
estrogen
on
ovarian
granulosa
cell
proliferation
by
upregulating
the
genes
of
c-
Myc
and
TERT
in
vivo
.
Estrogen
deficiency
or
over-activity
may
cause
ovarian
tissue
aging
or
tumorigenesis
,
respectively
,
through
estrogen
regulation
of
telomere
remodeling
.
Diseases
Validation
Diseases presenting
"tumorigenesis"
symptom
aromatase deficiency
esophageal squamous cell carcinoma
werner syndrome
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