BMSC‑derived exosome‑mediated miR‑25‑3p delivery protects against myocardial ischemia/reperfusion injury by constraining M1‑like macrophage polarization
Molecular Medicine Reports,
Год журнала:
2024,
Номер
30(2)
Опубликована: Июнь 18, 2024
Myocardial
ischemia/reperfusion
injury
(MIRI)
is
a
significant
challenge
in
the
management
of
myocardial
ischemic
disease.
Extensive
evidence
suggests
that
macrophage‑mediated
inflammatory
response
may
play
vital
role
MIRI.
Mesenchymal
stem
cells
and,
particular,
exosomes
derived
from
these
cells,
be
key
mediators
and
repair.
However,
whether
protect
heart
by
regulating
polarization
macrophages
exact
mechanisms
involved
are
poorly
understood.
The
present
study
aimed
to
determine
secreted
bone
marrow
mesenchymal
(BMSC‑Exo)
harboring
miR‑25‑3p
can
alter
phenotype
affecting
JAK2/STAT3
signaling
pathway,
which
reduces
protects
against
An
in
vivo
MIRI
model
was
established
rats
ligating
anterior
descending
region
left
coronary
artery
for
30
min
followed
reperfusion
120
min,
BMSC‑Exo
carrying
(BMSC‑Exo‑25‑3p)
were
administered
through
tail
vein
injection.
A
hypoxia‑reoxygenation
H9C2
established,
cocultured
with
BMSC‑Exo‑25‑3p
vitro.
results
demonstrated
or
could
taken
up
cardiomyocytes
powerful
cardioprotective
effects
decreasing
cardiac
infarct
size,
reducing
incidence
malignant
arrhythmias
attenuating
enzyme
activity,
as
indicated
lactate
dehydrogenase
creatine
kinase
levels.
It
induced
M1‑like
macrophage
after
(I/R),
evidenced
increase
iNOS
expression
immunofluorescence
staining
upregulation
proinflammatory
cytokines
RT‑qPCR,
such
interleukin‑1β
(IL‑1β)
interleukin‑6
(IL‑6).
As
hypothesized,
inhibited
cytokine
while
promoting
M2‑like
polarization.
Mechanistically,
pathway
activated
I/R
LPS‑stimulated
vitro,
pretreatment
this
activation.
indicate
attenuation
related
inactivation
subsequent
inhibition
Язык: Английский
p16INK4a Aggravated Sepsis-associated Cardiac Injury by Inhibiting the PI3K/AKT Pathway and Inducing Redox Imbalance
Journal of Cardiovascular Translational Research,
Год журнала:
2025,
Номер
unknown
Опубликована: Янв. 14, 2025
Язык: Английский
Innovative Approaches in Atherosclerosis Treatment: Harnessing Traditional Chinese Medicine to Target Long Non-Coding RNAs
Phytomedicine,
Год журнала:
2025,
Номер
139, С. 156488 - 156488
Опубликована: Фев. 9, 2025
Язык: Английский
Construction and diagnostic efficacy assessment of the urinary exosomal miRNA‐mRNA network in children with IgA vasculitis nephritis
The FASEB Journal,
Год журнала:
2025,
Номер
39(7)
Опубликована: Апрель 1, 2025
Abstract
This
study
aimed
to
comprehensively
evaluate
the
diagnostic
potential
of
urinary
exosomal
microRNA
(miRNA)
in
IgA
vasculitis
(IgAV)
kidney
injury
by
meticulously
comparing
miRNA
expression
profiles
urine
exosomes
between
children
diagnosed
with
IgAV
and
those
nephritis
(IgAVN).
Urine
samples
were
obtained
from
who
treated
at
our
hospital
October
2022
2023.
These
then
categorized
into
group
IgAVN
group.
High‐throughput
sequencing
bioinformatics
analysis
techniques
employed
conduct
a
thorough
differentially
expressed
miRNAs
two
groups.
Additionally,
correlation
clinical
parameters
was
evaluated.
A
total
57
exhibited
differential
Specifically,
group,
42
upregulated,
while
15
downregulated.
Lasso
regression
ROC
identified
five
candidate
high
accuracy.
prediction
95
target
genes
related
led
construction
an
miRNA‐mRNA
regulatory
network
consisting
four
key
ten
hub
genes.
Gene
function
metabolic
pathway
analyses
indicated
that
these
predominantly
enriched
pro‐fibrotic
inflammatory
pathways.
The
incorporating
demonstrated
significant
hsa‐miR‐383‐5p
protein
levels.
research
mRNAs
patterns
associated
constructed
corresponding
network.
It
determined
hsa‐miR‐3065‐5p,
hsa‐miR‐383‐5p,
hsa‐miR‐25‐3p,
hsa‐miR‐450b‐5p
might
mediate
pathogenesis
targeting
Among
them,
is
highly
likely
serve
as
novel
non‐invasive
biomarker
for
assessing
disease
status
IgAVN,
thereby
offering
new
perspectives
on
diagnosis
treatment
IgAVN.
Язык: Английский
LINC01270 Regulates the NF-κB-Mediated Pro-inflammatory Response via the miR-326/LDOC1 Axis in THP-1 Cells
Опубликована: Июнь 24, 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-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.
Язык: Английский
New insights into the function and therapeutic potential of RNA-binding protein TRBP in viral infection, chronic metabolic diseases, brain disorders and cancer
Life Sciences,
Год журнала:
2024,
Номер
unknown, С. 123159 - 123159
Опубликована: Окт. 1, 2024
Язык: Английский
LINC01270 Regulates the NF-κB-Mediated Pro-Inflammatory Response via the miR-326/LDOC1 Axis in THP-1 Cells
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.
Язык: Английский