Abstract
During
uterine
spiral
artery
remodeling,
vascular
smooth
muscle
cells
(VSMCs)
become
disorganized
and
undergo
phenotypic
switching
from
a
contractile
to
more
synthetic
phenotype.
We
have
previously
reported
that
natural
killer
induce
this
VSMC
by
secreting
angiopoietin‐2
(Ang‐2).
Here,
we
identified
the
specific
mechanisms
which
Ang‐2
plays
role
in
phenomenon.
VSMCs
isolated
human
umbilical
arteries
were
used
as
an
vitro
model
investigate
of
switching.
Human
decidua
tissue
preeclamptic
control
pregnancies
was
collected
compare
expression
levels
related
proteins.
induced
phenotype
evidenced
decreased
marker
expression,
increased
proliferation
migration,
altered
cytoskeleton.
expressed
integrin
β6
interacted
directly
with
phosphorylation
FAK
(S910
Y397),
AKT
(S473),
mTOR
(S2448).
Knockdown
recovered
calponin
loss
resulted
lower
EZH2
abundance.
Inhibition
both
attenuated
Ang‐2‐induced
inhibition
LC3
II/LC3
I
ratio
ATG7
proliferation.
Lipid
peroxidation
ferrostatin‐1
or
IL‐8
receptor
antagonist
navarixin
inhibited
migration.
secretion
significantly
lipid
inhibition.
In
decidua,
there
unremodeled
arteries,
abundance
dysregulated.
dysregulation
may
disrupt
remodeling
contribute
preeclampsia.
be
novel
therapeutic
target
for
treatment
pregnancy
complications
affected
incomplete
remodeling.
Frontiers in Immunology,
Год журнала:
2025,
Номер
15
Опубликована: Янв. 7, 2025
We
aim
to
explore
the
immunomodulatory
properties
of
T
cells
on
different
titanium
nanotubes
and
key
immunological
factors
involved
in
this
process.
Transcriptome
data
from
GEO
database
healthy
people
implants
were
used
analyze
cell
infiltration
factor
distribution
adaptive
immune
using
bioinformatics
tools.
activated
rat
cultured
that
prepared
by
anodization
with
diameters
(P-0,
NT15-30
nm,
NT40-100
NT70-200
nm).
The
proliferation
expressions
main
transcription
cytokines
T-cells
detected.
Magnetic
bead
sorting
CD3+
transcriptome
sequencing
performed
signaling
pathways
may
influence
related
responses.
Bioinformatics
analysis
showed
peri-implant
tissues
enriched
most
T-cell
subtypes.
T-cell-mediated
responses
IL-17A.
On
third
day,
NT15
NT40
groups
significantly
higher
pro-proliferative
effects
than
NT70
group
(P<0.05).
Notably,
exhibited
lowest
T-bet
expression
(P<0.05)
along
highest
levels
Rorγt,
Gata3,
Foxp3(P<0.05),
followed
group.
Additionally,
demonstrated
reduced
RANKL,
TNF-α,
IL-6
increased
OPG
IL-10
Meanwhile,
had
lower
IFN-γ
expression(P>0.05)
but
IL-4,
TGF-β1
expressions(P<0.05).
Differential
expressed
genes
(DGEs)
morphologies
mostly
IL-17
pathway
mediated
IL-17A/F.
Gene
protein
indicated
secretion
IL-17A
cells.
Titanium
nanotube
medium
(100
nm)
small
(30
sizes
differentiation
secretion,
T-cell-derived
likely
playing
a
regulatory
role.
Frontiers in Immunology,
Год журнала:
2025,
Номер
15
Опубликована: Янв. 13, 2025
Ferroptosis,
a
recently
discovered
iron-dependent
cell
death,
is
linked
to
various
diseases
but
its
role
in
endometriosis
still
not
fully
understood.
In
this
study,
we
integrated
microarray
data
of
from
the
GEO
database
and
ferroptosis-related
genes
(FRGs)
FerrDb
further
investigate
regulation
ferroptosis
impact
on
immune
microenvironment.
WGCNA
identified
modules,
annotated
by
GO
&
KEGG.
MNC
algorithm
pinpointed
hub
FRGs.
Cytoscape
construct
ceRNA
network,
ROC
curves
evaluated
diagnostic
efficacy
Consensus
cluster
analysis
subclusters,
CIBERSORT
assessed
infiltration
these
subclusters.
Finally,
RT-qPCR
validated
FRG
expression
clinical
tissues.
We
two
modules
endometriosis,
enrichment
analysis,
they
are
closely
with
autophagy,
mTOR,
oxidative
stress,
FOXO
pathways.
Furthermore,
10
FRGs,
curve
showed
better
predictive
ability
for
diagnosing.
confirmed
that
tissue
FRGs
was
mostly
consistent
results.
Subsequently,
developed
network
based
4
(BECN1,
OSBPL9,
TGFBR1,
GSK3B).
Next,
subclusters
stage.
Importantly,
illustrated
levels
cells
checkpoint
were
significantly
different
Specifically,
subcluster
stage
III-IV
more
inclined
immunosuppressive
Our
study
may
jointly
promote
progression
remodeling
microenvironment,
offering
new
insights
into
pathogenesis
therapeutics.
Scientific Reports,
Год журнала:
2025,
Номер
15(1)
Опубликована: Фев. 5, 2025
Abstract
Endometriosis
is
a
chronic
inflammatory
disease
characterized
by
the
presence
of
endometrial-like
tissues
(glands
and
stroma)
located
outside
uterine
cavity.
The
pathophysiology
this
condition
remains
incompletely
understood.
Local
bleeding
inflammation
within
endometriosis
lesions,
which
occur
in
an
environment
rich
iron,
reactive
oxygen
species
(ROS),
free
radicals,
can
disturb
balance
iron
peritoneal
This
disruption
trigger
oxidative
injury
response,
leading
to
ferroptosis,
particularly
endometrioma
phenotype.
research
utilized
observational
analytical
method
with
cross-sectional
design
examine
relationship
between
ferritin
GPx4
levels
assessing
them
simultaneously.
data
collection
occurred
at
Dr.
Hasan
Sadikin
Hospital,
Cibabat
Bandung
Kiwari
Limijati
Women
Children
Hospital
Bandung.
Observational
analytic
were
gathered
February
July
2023
from
female
patients
diagnosed
who
underwent
either
laparoscopic
or
laparotomy
surgery,
for
therapeutic
diagnostic
reasons.
There
58
met
inclusion
exclusion
criteria
study.
A
significant
correlation
was
observed
glutathione
peroxidase
4
(GPx4)
coefficient
-0.600
(
p
<
0.001).
However,
there
no
both
severity
(based
on
Association
Gynecologic
Laparoscopists
staging).
levels.
Abstract
During
uterine
spiral
artery
remodeling,
vascular
smooth
muscle
cells
(VSMCs)
become
disorganized
and
undergo
phenotypic
switching
from
a
contractile
to
more
synthetic
phenotype.
We
have
previously
reported
that
natural
killer
induce
this
VSMC
by
secreting
angiopoietin‐2
(Ang‐2).
Here,
we
identified
the
specific
mechanisms
which
Ang‐2
plays
role
in
phenomenon.
VSMCs
isolated
human
umbilical
arteries
were
used
as
an
vitro
model
investigate
of
switching.
Human
decidua
tissue
preeclamptic
control
pregnancies
was
collected
compare
expression
levels
related
proteins.
induced
phenotype
evidenced
decreased
marker
expression,
increased
proliferation
migration,
altered
cytoskeleton.
expressed
integrin
β6
interacted
directly
with
phosphorylation
FAK
(S910
Y397),
AKT
(S473),
mTOR
(S2448).
Knockdown
recovered
calponin
loss
resulted
lower
EZH2
abundance.
Inhibition
both
attenuated
Ang‐2‐induced
inhibition
LC3
II/LC3
I
ratio
ATG7
proliferation.
Lipid
peroxidation
ferrostatin‐1
or
IL‐8
receptor
antagonist
navarixin
inhibited
migration.
secretion
significantly
lipid
inhibition.
In
decidua,
there
unremodeled
arteries,
abundance
dysregulated.
dysregulation
may
disrupt
remodeling
contribute
preeclampsia.
be
novel
therapeutic
target
for
treatment
pregnancy
complications
affected
incomplete
remodeling.