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Down regulation of miR-124 in both Werner syndrome DNA helicase mutant mice and mutant Caenorhabditis elegans wrn-1 reveals the importance of this microRNA in accelerated aging.
[werner syndrome]
Small
non-coding
microRNAs
are
believed
to
be
involved
in
the
mechanism
of
aging
but
nothing
is
known
on
the
impact
of
microRNAs
in
the
progeroid
disorder
Werner
syndrome
(
WS
)
.
WS
is
a
premature
aging
disorder
caused
by
mutations
in
a
RecQ-like
DNA
helicase
.
Mice
lacking
the
helicase
domain
of
the
WRN
ortholog
exhibit
many
phenotypic
features
of
WS
,
including
a
pro-oxidant
status
and
a
shorter
mean
life
span
.
Caenorhabditis
elegans
(
C
.
elegans
)
with
a
nonfunctional
wrn-
1
DNA
helicase
also
exhibit
a
shorter
life
span
.
Thus
,
both
models
are
relevant
to
study
the
expression
of
microRNAs
involved
in
WS
.
In
this
study
,
we
show
that
miR-
124
expression
is
lost
in
the
liver
of
Wrn
helicase
mutant
mice
.
Interestingly
,
the
expression
of
this
conserved
miR-
124
in
whole
wrn-
1
mutant
worms
is
also
significantly
reduced
.
The
loss
of
mir-
124
in
C
.
elegans
increases
reactive
oxygen
species
formation
and
accumulation
of
the
aging
marker
lipofuscin
,
reduces
whole
body
ATP
levels
and
results
in
a
reduction
in
life
span
.
Finally
,
supplementation
of
vitamin
C
normalizes
the
median
life
span
of
wrn-
1
and
mir-
124
mutant
worms
.
These
results
suggest
that
biological
pathways
involving
WRN
and
miR-
124
are
conserved
in
the
aging
process
across
different
species
.