Cells,
Год журнала:
2023,
Номер
12(14), С. 1821 - 1821
Опубликована: Июль 11, 2023
Osteoarthritis
(OA)
is
a
joint
disorder
characterized
by
progressive
degeneration
of
cartilage
extracellular
matrix
(ECM),
chondrocyte
hypertrophy
and
apoptosis
inflammation.
The
current
treatments
mainly
concern
pain
control
reduction
inflammation,
but
no
therapeutic
strategy
has
been
identified
as
disease-modifying
treatment.
Therefore,
identifying
specific
biomarkers
useful
to
prevent,
treat
or
distinguish
the
stages
OA
disease
become
an
immediate
need
clinical
practice.
role
microRNAs
(miRNAs)
in
investigated
last
decade,
increasing
evidence
emerged
that
influence
environment
on
gene
expression
through
epigenetic
processes
contributes
development,
progression
aggressiveness
OA,
particular
acting
microenvironment
modulations.
effects
regulation,
particularly
different
miRNA
methylation
during
disease,
were
highlighted
present
systematic
review.
arising
from
this
study
literature
conducted
three
databases
(PubMed,
Scopus,
Web
Science)
suggested
state
already
strongly
impacts
progression,
driving
chondrocytes
synoviocyte
proliferation,
apoptosis,
inflammation
ECM
deposition.
However,
possibility
understanding
mechanism
which
modifications
pre-miRNA
sequences
drive
could
be
new
focus
future
investigations.
Objective
Temporomandibular
joint
osteoarthritis
(TMJOA)
seriously
influences
the
quality
of
life
patients.
Chondrocyte
mitochondrial
dysfunction
and
pyroptosis
play
an
important
role
in
development
osteoarthritis,
but
their
TMJOA
pathogenesis
is
elusive.
We
aimed
to
probe
into
mechanism
TMJOA.
Design
rat
models
were
established
by
unilateral
anterior
crossbite
operation.
Pathological
changes
cartilage
tissues
observed
hematoxylin-eosin
staining,
evaluated
immunohistochemistry.
The
biological
function
ZC3H13
determined
cell
experiments.
Results
discovered
that
occurred
rats.
expression
was
observably
upregulated
Further
experiments
showed
interference
restrained
chondrocytes.
RNA
sequencing
revealed
NSUN4
significantly
increased
chondrocytes
after
knockdown.
Silencing
remarkably
diminished
level
N6-methyladenosine
(m6A)
modification.
Moreover,
notably
Conclusion
Our
study
ZC3H13-mediated
repressed
progression
modulating
chondrocyte
m6A-dependent
manner,
which
may
offer
a
potential
strategy
for
treatment.
Ecotoxicology and Environmental Safety,
Год журнала:
2023,
Номер
263, С. 115265 - 115265
Опубликована: Июль 19, 2023
Nicotine
contributes
to
the
causation
of
atherosclerosis,
which
prominent
cellular
components
are
macrophages.
Long
non-coding
RNAs
(lncRNAs)
play
an
important
role
in
regulating
cell
functions
such
as
proliferation,
differentiation
and
programmed
death.
However,
function
mechanism
lncRNAs
nicotine-induced
macrophage
pyroptosis
has
not
been
reported.
We
screened
deferentially
expressed
human
carotid
artery
plaque
(GSE97210)
verified
them
Results
showed
only
LINC01272
was
up-regulated
a
dose-dependent
manner
The
immunofluorescence
staining
result
confirmed
that
interfering
inhibited
pyroptosis.
Through
bioinformatics
analysis,
dual
luciferase
reporter
gene
assay
qPCR,
we
identified
miR-515
significantly
negatively
correlated
with
expression
LINC01272,
KLF6
is
target
miR-515.
Furthermore,
our
results
demonstrated
LINC01272/miR-515/KLF6
axis
meditated
In
addition,
peripheral
blood
mononuclear
cells
smoking
populations,
GSDMD-N,
NLRP3,
increased,
while
level
reduced.
This
study
nicotine
increases
competitively
bind
macrophages,
reducing
inhibitory
effect
on
its
KLF6,
ultimately
induces
Journal of Orthopaedic Surgery and Research,
Год журнала:
2023,
Номер
18(1)
Опубликована: Сен. 18, 2023
Knee
osteoarthritis
(KOA)
is
characterized
by
joint
wear
and
degeneration.
Unfortunately,
the
medical
community
currently
lacks
effective
treatment
options
for
this
disease.
Suspension
exercise
therapy
considered
an
form
of
non-weight-bearing
treating
KOA.
However,
its
mechanism
intervention
in
KOA
unclear.
Therefore,
study
aimed
to
evaluate
protective
effects
on
rats
with
attempted
explore
underlying
mechanisms.In
study,
a
papain-induced
model
was
constructed,
pathological
changes
cartilage
tissue
were
observed
hematoxylin
eosin
(H&E)
staining
scored
according
Mankin
scoring
principle.
The
serum
levels
interleukin
(IL)-1β,
IL-6,
tumor
necrosis
factor-α
(TNF-α)
detected
enzyme-linked
immunosorbent
assay.
Reverse
transcription-quantitative
polymerase
chain
reaction
Western
blotting
used
detect
expression
mRNA
proteins
TLR4/MyD88/NF-κB
signaling
pathway.H&E
score
data
confirmed
that
significantly
improved
articular
degradation
compared
group.
Further,
we
differentially
reduced
IL-1β,
TNF-α.
Mechanistically,
downregulated
gene
protein
TLR4,
MyD88,
NF-κB
tissue.Non-weight-bearing
resulted
progression
modulating
pathway
decreasing
inflammatory
cytokines
TNF-α
slow
down
degeneration
cartilage.
Frontiers in Immunology,
Год журнала:
2023,
Номер
14
Опубликована: Март 16, 2023
Background
Osteoarthritis
(OA)
is
the
most
common
joint
degenerative
disease,
and
so
far,
there
no
effective
therapy
to
prevent
or
delay
its
development.
Considerable
attention
now
being
given
impact
of
m6A
RNA
methylation
modification
on
disease
immune
regulation.
However,
much
remains
unknown
about
function
in
OA.
Methods
A
total
63
OA
59
healthy
samples
were
applied
comprehensively
examine
regulators
mediated
pattern
OA,
evaluate
impacts
distinct
patterns
characteristics
microenvironment,
including
infiltration
cells,
responses
human
leukocyte
antigen
(HLAs)
genes
expression.
In
addition,
we
screened
out
phenotype-related
further
explored
their
potential
biological
functions.
At
last,
verified
expression
key
associations
with
vitro
.
Results
Most
was
differentially
expressed
compared
normal
tissues.
Based
six
hub-m6A
identified
as
abnormally
samples,
developed
a
classifier
distinguish
patients
from
individuals.
We
noted
that
correlated
regulators.
For
instance,
YTHDF2
had
strongest
significantly
positive
correlation
regulatory
T
cells
(Tregs)
IGFBP2
negatively
associated
dendritic
(DCs),
which
confirmed
by
immunohistochemistry
(IHC)
staining.
Two
determined:
B
higher
infiltrating
immunocytes
more
active
than
A,
two
differed
HLA
genes.
also
1,592
could
mediate
synovitis
cartilage
degradation
PI3K-Akt
signaling
pathway.
Quantitative
real-time
polymerase
chain
reaction
(qRT-PCR)
results
indicated
overexpressed,
while
mRNA
decreased
consistent
our
findings.
Conclusion
Our
research
proves
essential
helps
explain
mechanism
behind
it,
may
open
up
new
direction
for
precise
immunotherapy
osteoarthritis.
Cells,
Год журнала:
2023,
Номер
12(14), С. 1821 - 1821
Опубликована: Июль 11, 2023
Osteoarthritis
(OA)
is
a
joint
disorder
characterized
by
progressive
degeneration
of
cartilage
extracellular
matrix
(ECM),
chondrocyte
hypertrophy
and
apoptosis
inflammation.
The
current
treatments
mainly
concern
pain
control
reduction
inflammation,
but
no
therapeutic
strategy
has
been
identified
as
disease-modifying
treatment.
Therefore,
identifying
specific
biomarkers
useful
to
prevent,
treat
or
distinguish
the
stages
OA
disease
become
an
immediate
need
clinical
practice.
role
microRNAs
(miRNAs)
in
investigated
last
decade,
increasing
evidence
emerged
that
influence
environment
on
gene
expression
through
epigenetic
processes
contributes
development,
progression
aggressiveness
OA,
particular
acting
microenvironment
modulations.
effects
regulation,
particularly
different
miRNA
methylation
during
disease,
were
highlighted
present
systematic
review.
arising
from
this
study
literature
conducted
three
databases
(PubMed,
Scopus,
Web
Science)
suggested
state
already
strongly
impacts
progression,
driving
chondrocytes
synoviocyte
proliferation,
apoptosis,
inflammation
ECM
deposition.
However,
possibility
understanding
mechanism
which
modifications
pre-miRNA
sequences
drive
could
be
new
focus
future
investigations.
