Multiple Sclerosis: Roles of miRNA, lcnRNA, and circRNA and Their Implications in Cellular Pathways
International Journal of Molecular Sciences,
Год журнала:
2024,
Номер
25(4), С. 2255 - 2255
Опубликована: Фев. 13, 2024
Multiple
sclerosis
(MS)
is
a
degenerative
condition
characterized
by
axonal
damage
and
demyelination
induced
autoreactive
immune
cells
that
occur
in
the
Central
Nervous
System
(CNS).
The
interaction
between
epigenetic
changes
genetic
factors
can
be
widely
involved
onset,
development,
progression
of
disease.
Although
numerous
efforts
were
made
to
discover
new
therapies
able
prevent
improve
course
MS,
definitive
curative
treatments
have
not
been
found
yet.
However,
recent
years,
it
has
reported
non-coding
RNAs
(ncRNAs),
including
microRNAs
(miRNAs),
long
ncRNAs
(lncRNAs),
circular
(circRNAs),
acting
as
gene
expression
regulators,
could
used
potential
therapeutic
targets
or
biomarkers
diagnose
fight
MS.
In
this
review,
we
discussed
role
miRNAs,
lncRNAs,
circRNAs,
well
their
level
signaling
pathways
are
related
preclinical
human
MS
studies.
Hence,
investigation
important
provide
additional
information
regarding
pathogenesis
promote
discovery
strategies
biomarkers.
Язык: Английский
Dysregulation of LINC01094 is involved in the pathogenesis of pulpitis by regulating the miR-340-5p expression
Odontology,
Год журнала:
2025,
Номер
unknown
Опубликована: Янв. 9, 2025
Язык: Английский
Epigenetic and Mitochondrial Metabolic Dysfunction in Multiple Sclerosis: A Review of Herbal Drug Approaches and Current Clinical Trials
Molecular Neurobiology,
Год журнала:
2025,
Номер
unknown
Опубликована: Апрель 3, 2025
Язык: Английский
Single-cell sequencing reveals glial cell involvement in development of neuropathic pain via myelin sheath lesion formation in the spinal cord
Journal of Neuroinflammation,
Год журнала:
2024,
Номер
21(1)
Опубликована: Авг. 31, 2024
Neuropathic
pain
(NP),
which
results
from
injury
or
lesion
of
the
somatosensory
nervous
system,
is
intimately
associated
with
glial
cells.
The
roles
microglia
and
astrocytes
in
NP
have
been
broadly
described,
while
studies
on
oligodendrocytes
largely
focused
axonal
myelination.
mechanisms
their
interactions
other
cells
development
remain
uncertain.
Язык: Английский
Short-chain fatty acids abrogate Japanese encephalitis virus-induced inflammation in microglial cells via miR-200a-3p/ZBTB20/IKβα axis
Atreye Majumdar,
Indira Priya Siva Venkatesh,
Vivek Swarup
и другие.
mBio,
Год журнала:
2024,
Номер
15(7)
Опубликована: Июнь 13, 2024
Japanese
encephalitis
virus
(JEV),
a
member
of
the
Flaviviridae
family,
is
leading
cause
viral
in
humans.
Survivors
this
infection
often
develop
lifelong
neurological
sequelae.
Short-chain
fatty
acids
(SCFAs)
produced
gut
are
vital
mediators
gut-brain
axis.
We
aimed
to
study
microRNA-based
mechanisms
SCFAs
an
vitro
model
JEV
infection.
N9
microglial
cells
were
pretreated
with
SCFA
cocktail
before
Cytokine
bead
analysis,
immunoblotting,
and
PCR
performed
analyze
relevant
inflammatory
markers.
microRNA
sequencing
was
using
Illumina
Hiseq,
bioinformatics
tools
used
for
differentially
expressed
(DE)
miRNAs
weighted
gene
co-expression
network
analysis
(WGCNA).
mimic/inhibitor
experiments
luciferase
assay
miRNA-target
interaction.
A
significant
reduction
monocyte
chemoattractant
protein
(MCP1)
tumor
necrosis
factor
alpha
(TNFα)
along
reduced
expression
phospho-nuclear
kappa
B
(phospho-NF-κB)
observed
conditions.
Significant
attenuation
histone
deacetylase
activity
recorded.
miRNA
revealed
160
DE
+
JEV-treated
at
6
h
post-infection.
WGCNA
miR-200a-3p,
hub
significantly
upregulated
Transcription
ZBTB20
bioinformatically
predicted
validated
as
target
miR-200a-3p.
Further
demonstrated
that
miR-200-3p
regulated
Iκβα
possibly
dampened
NF-κB
signal
activation
downstream.
The
axis
plays
pivotal
role
physiological
state
organism.
Gut
microbiota-derived
metabolites
known
play
brain
disorders
including
neuroviral
infections.
appear
quench
markers
virus-infected
vitro.
Mechanistically,
we
demonstrate
interaction
between
miR-200a-3p
regulating
canonical
nuclear
(NF-κB)
signaling
pathway
via
transcriptional
regulation
Iκβα.
Findings
pave
way
better
understanding
can
be
strategies
against
neuroinflammation.
Язык: Английский
MicroRNAs dysregulated in multiple sclerosis affect the differentiation of CG-4 cells, an oligodendrocyte progenitor cell line
Frontiers in Cellular Neuroscience,
Год журнала:
2024,
Номер
18
Опубликована: Фев. 29, 2024
Introduction
Demyelination
is
one
of
the
hallmarks
multiple
sclerosis
(MS).
While
remyelination
occurs
during
disease,
it
incomplete
from
start
and
strongly
decreases
with
its
progression,
mainly
due
to
harm
oligodendrocyte
progenitor
cells
(OPCs),
causing
irreversible
neurological
deficits
contributing
neurodegeneration.
Therapeutic
strategies
promoting
are
still
very
preliminary
lacking
within
current
treatment
panel
for
MS.
Methods
In
a
previous
study,
we
identified
21
microRNAs
dysregulated
mostly
in
CSF
relapsing
and/or
remitting
MS
patients.
this
study
transfected
mimics/inhibitors
several
these
separately
an
OPC
cell
line,
called
CG-4.
We
aimed
(1)
phenotypically
characterize
their
effect
on
differentiation
(2)
identify
corroborating
potential
mRNA
targets
via
immunocytochemistry,
RT-qPCR
analysis,
RNA
sequencing,
Gene
Ontology
enrichment
analysis.
Results
observed
that
majority
13
microRNA
mimics
decreased
CG-4
cells.
demonstrate,
by
sequencing
independent
analyses,
miR-33-3p,
miR-34c-5p,
miR-124-5p
arrest
at
late
stage
miR-145-5p
premyelinating
as
evidenced
downregulation
(OL)
[
Tcf7l2
,
Cnp
(except
miR-145-5p)]
mature
OL
(
Plp1
Mbp
Mobp
)
markers,
whereas
only
miR-214-3p
promotes
differentiation.
further
propose
comprehensive
exploration
change
fate
through
finally
confirm
analyses
predicted
each
possibly
support
distinctive
mechanisms,
which
some
unexplored
OPC/OL
physiology.
Conclusion
stage,
hypothetical
mechanisms
exerts
effect.
hereby
open
new
perspectives
research
pathophysiology
demyelination/remyelination,
even
search
remyelinating
therapeutic
scope
Язык: Английский
Unveiling the Molecular Network of Oxidative Stress in Coronary Artery Disease Pathogenesis: Evidence from Multi-Omics Mendelian Randomization Study
Опубликована: Янв. 1, 2024
Background:
Coronary
artery
disease
(CAD)
poses
a
significant
health
threat,
with
oxidative
stress
(OS)
emerging
as
an
essential
pathophysiological
mechanism.
Unveiling
the
interaction
between
OS
and
CAD
pathogenesis
is
crucial
for
effective
prevention
therapeutic
interventions.Methods:
A
multi-omics
strategy
was
employed
to
investigate
underlying
associations
genes
CAD.
Transcriptomic
datasets
related
were
collected
from
Gene
Expression
Omnibus
(GEO)
database.
We
performed
differential
expression
analysis
identify
differentially
expressed
(DEGs)
associated
in
CAD,
followed
by
meta-analysis
consolidate
findings.
Integrating
genome-wide
association
study
(GWAS)
summary
statistics
quantitative
trait
loci
(eQTLs)
DNA
methylation
QTLs
(mQTLs)
blood,
we
utilized
three-step
data-based
Mendelian
randomization
(SMR)
probe
preferential
their
regulatory
elements
that
correlated
susceptibility.
further
SMR
colocalization
unveil
potential
interplay
host
gene
gut
microbiota
relation
incorporation
of
blood
eQTLs,
intestinal
eQTLs
fecal
(mbQTLs).Findings:
total
129
OS-related
DEGs
identified
via
context
Leveraging
analysis,
seven
CAD:
SREBF1,
PDE5A,
MAPKAP1,
SMARCA4,
CSNK2A1,
OPA1
VARS2,
two
which
mediated
(DNAm)
regulation
on
expression:
SREBF1
MAPKAP1.
Furthermore,
integration
prioritized
three
putative
CAD-causal
tissues:
ARNT
TSFM,
all
presented
evidence
host-microbiota
interactions.Interpretation:
This
causally
highlighted
mechanisms
involving
DNAm
interactions.
These
findings
provide
insight
into
role
targets
treatment
this
disease.Funding:
project
supported
National
Natural
Science
Foundation
China
(No.
82074254,
82374281),
Beijing
(No.7172185),
Independent
Innovation
Capital
Health
Development
Scientific
Research
Project
(2024-2-4154),
Technological
Academy
Chinese
Medical
Sciences
(C12021A01413).Declaration
Interest:
The
authors
declare
they
have
no
competing
interests.
Язык: Английский
LINC01094: A Key Long Non-Coding RNA in the Regulation of Cancer Progression and Therapeutic Targets
Heliyon,
Год журнала:
2024,
Номер
10(18), С. e37527 - e37527
Опубликована: Сен. 1, 2024
LINC01094
is
a
long
non-coding
RNA
that
plays
crucial
role
in
cancer
progression
by
modulating
key
signaling
pathways,
such
as
PI3K/AKT,
Wnt/β-catenin
and
TGF-β
Signaling
Pathway
Feedback
Loop.
In
this
review
we
summarize
the
recent
research
on
functional
mechanisms
of
various
cancers,
including
its
impact
tumor
growth,
metastasis,
resistance
to
therapy.
We
also
discuss
therapeutic
potential
targeting
highlight
current
strategies
challenges
area.
Perspectives
future
development
LINC01094-based
therapies
are
provided.
Язык: Английский