Cells,
Год журнала:
2024,
Номер
13(23), С. 2027 - 2027
Опубликована: Дек. 8, 2024
Long
intergenic
noncoding
(LINC)01270
is
a
2278
bp
transcript
belonging
to
the
subset
of
long
(lnc)RNAs.
Despite
increased
reports
LINC01270's
involvement
in
different
diseases,
evident
research
on
its
effects
inflammation
yet
be
achieved.
In
present
study,
we
investigated
potential
role
LINC01270
modulating
inflammatory
response
human
monocytic
leukemia
cell
line
THP-1.
Lipopolysaccharide
treatment
upregulated
expression,
and
siRNA-mediated
suppression
enhanced
NF-κB
activity
subsequent
production
cytokines
IL-6,
IL-8,
MCP-1.
Interestingly,
knockdown
downregulated
expression
leucine
zipper
cancer
1
(LDOC1),
novel
suppressor.
An
analysis
LINC01270/micro-RNA
(miRNA)/protein
interactome
profile
identified
miR-326
as
possible
mediator.
Synthetic
RNA
agents
that
perturb
interaction
among
LINC01270,
miR-326,
LDOC1
mRNA
mitigated
changes
caused
by
THP-1
cells.
Additionally,
luciferase
reporter
assay
HEK293
cells
further
confirmed
enhances
activation,
while
overexpression
has
opposite
effect.
This
study
provides
insight
into
responses
lipopolysaccharide
stimulation
via
miR-326/LDOC1
axis,
which
negatively
regulates
activation.
International Journal of Molecular Sciences,
Год журнала:
2025,
Номер
26(2), С. 560 - 560
Опубликована: Янв. 10, 2025
Rheumatoid
arthritis
(RA)
is
a
chronic
autoimmune
disease
that
leads
to
joint
damage
and
physical
dysfunction.
The
pathogenesis
of
RA
highly
complex,
involving
genetic,
epigenetic,
immune,
metabolic
factors,
among
others.
Over
the
years,
research
has
highlighted
importance
non-coding
RNAs
(ncRNAs)
in
regulating
gene
expression.
Given
their
dysregulation
numerous
conditions,
ncRNAs
are
thought
play
role
pathological
processes.
In
RA,
aberrant
levels
circulating
long
(lncRNAs)
commonly
observed
peripheral
blood,
along
with
dysregulated
expression
blood
mononuclear
cells
synovial
tissue.
This
review
discusses
involvement
lncRNAs
inflammation
aggressive
characteristics
fibroblast-like
synoviocytes,
key
cellular
population
driving
progression.
Frontiers in Immunology,
Год журнала:
2025,
Номер
16
Опубликована: Фев. 19, 2025
The
NLRP3
inflammasome
and
NF-κB
signaling
pathways
play
crucial
roles
in
orchestrating
inflammation
immune
defense.
This
review
explores
the
intricate
relationship
between
these
epigenetic
regulation,
a
field
of
growing
importance
understanding
responses.
Epigenetic
modifications,
including
DNA
methylation,
histone
non-coding
RNAs
(ncRNAs),
significantly
influence
activity
genes
involved
pathways,
thereby
modulating
inflammatory
provides
comprehensive
overview
current
research
on
how
mechanisms
interact
with
regulate
pathways.
It
delves
into
advanced
concepts
such
as
RNA
modifications
3D
genome
organization,
their
impact
regulation.
Furthermore,
implications
findings
for
developing
novel
therapeutic
strategies
targeting
regulators
diseases
are
discussed.
By
synthesizing
recent
advancements
this
rapidly
evolving
field,
underscores
critical
role
regulation
highlights
potential
epigenetic-based
therapies
treating
wide
range
conditions,
autoimmune
disorders
cancer.
Long
intergenic
noncoding
(LINC)01270
is
a
2278
bp
transcript
belonging
to
the
subset
of
long
(lnc)RNAs.
Despite
increased
reports
LINC01270’s
involvement
in
different
diseases,
evident
research
on
its
effects
inflammation
yet
be
achieved.
In
present
study,
we
investigated
potential
role
LINC01270
modulating
inflammatory
response
human
monocytic
leukemia
cell
line
THP-1.
Lipopolysaccharide
treatment
upregulated
expression,
and
siRNA-mediated
suppression
enhanced
NF-kB
activity
subsequent
production
cytokines
IL-6,
IL-8,
MCP-1.
Interestingly,
knockdown
downregulated
expression
leucine
zipper
cancer
1
(LDOC1),
novel
suppressor.
An
analysis
LINC01270/micro-RNA
(miRNA)/protein
interactome
profile
identified
miR-326
as
possible
mediator.
Synthetic
RNA
agents
that
perturb
interaction
among
LINC01270,
miR-326,
LDOC1
mRNA
mitigated
changes
caused
by
THP-1
cells.
Additionally,
luciferase
re-porter
assay
HEK293
cells
further
confirmed
enhances
activation,
while
overexpression
has
opposite
effect.
This
study
provides
insight
into
responses
lipopolysaccharide
stimulation
via
miR-326/LDOC1
axis
which
negatively
regulates
activation.
Frontiers in Pharmacology,
Год журнала:
2024,
Номер
15
Опубликована: Окт. 9, 2024
Introduction
Nuclear
factor
kappa
B
(NF-κB)
is
a
key
regulator
of
immune
and
inflammatory
responses.
Glucocorticoid
drugs
(GC)
act
through
the
glucocorticoid
receptor
(GR)
as
immunosuppressant
also
in
pediatric
patients
inhibiting
NF-κB
activity.
The
long
non-coding
RNA
GAS5
interacts
with
GR,
influencing
GC
No
data
on
role
GR-dependent
inhibition
activity
have
been
published.
Methods
This
study
investigated
impact
HeLa
cells
overexpressing
GAS5,
both
under
basal
conditions
during
treatment.
used
EMSA,
RNA-immunoprecipitation
(RIP),
Western
blotting,
bioinformatic
analyses
to
assess
DNA
binding,
GAS5-p65
interaction,
signaling
pathway
modulation.
Results
overexpression
increased
binding
untreated
cells.
RNA-IP
confirmed
direct
interaction
between
subunit
p65,
suggesting
potential
regulatory
mechanism.
led
downregulation
target
genes,
TNF-α,
NR3C1.
treatment
reduced
GAS5-overexpressing
cells,
indicating
synergistic
effect.
Furthermore,
IκB
levels
p-p65/pan-p65
Discussion
appears
modulate
complex
manner,
GC-induced
signaling.
GCs,
multi-faceted,
further
research
needed
fully
elucidate
underlying
mechanisms.
These
findings
suggest
that
could
be
for
personalized
therapy,
particularly
conditions.
Scientific Reports,
Год журнала:
2024,
Номер
14(1)
Опубликована: Окт. 28, 2024
Long
non-coding
RNAs
(lncRNAs)
have
emerged
as
pivotal
regulators
in
numerous
biological
processes,
including
macrophage-mediated
inflammatory
responses,
which
play
a
critical
role
the
progress
of
diverse
diseases.
This
study
focuses
on
regulatory
function
lncRNA
brain
and
reproductive
organ-expressed
protein
(BRE)
antisense
RNA
1
(BRE-AS1)
modulating
activation
monocytes/macrophages.
Employing
THP-1
cell
line
model,
we
demonstrate
that
lipopolysaccharide
(LPS)
treatment
significantly
upregulates
BRE-AS1
expression.
Notably,
specific
knockdown
via
siRNA
transfection
enhances
LPS-induced
expression
interleukin
(IL)-6
IL-1β,
while
not
affecting
tumor
necrosis
factor
(TNF)-α
levels.
selective
augmentation
pro-inflammatory
cytokine
production
coincides
with
increased
phosphorylation
Janus
kinase
(JAK)2
signal
transducer
activator
transcription
(STAT)3.
Furthermore,
suppression
results
downregulation
suppressor
signaling
(SOCS)3,
an
established
inhibitor
JAK2/STAT3
pathway.
Bioinformatics
analysis
identified
binding
sites
for
miR-30b-5p
both
SOCS3
mRNA.
Intervention
synthetic
fragment
represents
site
attenuates
effects
knockdown.
Conversely,
mimic
replicated
attenuation
outcomes.
Our
findings
elucidate
cells
miR-30b-5p/SOCS3/JAK2/STAT3
pathway,
proposing
manipulation
macrophage
activity
may
offer
novel
therapeutic
avenue
diseases
characterized
by
macrophage-driven
pathogenesis.
