Clinical & Experimental Immunology,
Journal Year:
2021,
Volume and Issue:
205(1), P. 12 - 27
Published: March 27, 2021
Systemic
sclerosis
(SSc)
is
an
autoimmune
disease
characterized
by
significant
vascular
alterations
and
multi-organ
fibrosis.
Microvascular
are
the
first
event
of
SSc
injured
endothelial
cells
(ECs)
may
transdifferentiate
towards
myofibroblasts,
responsible
for
fibrosis
collagen
deposition.
This
process
identified
as
endothelial-to-mesenchymal
transition
(EndMT),
understanding
its
development
pivotal
to
identify
early
pathogenetic
events
new
therapeutic
targets
SSc.
In
this
review,
we
have
highlighted
molecular
mechanisms
EndMT
summarize
evidence
role
played
during
progressive
in
SSc,
also
exploring
possible
inhibition.
Journal of Experimental & Clinical Cancer Research,
Journal Year:
2023,
Volume and Issue:
42(1)
Published: July 6, 2023
Endothelial-mesenchymal
transition
(EndoMT)
is
an
emerging
adaptive
process
that
modulates
lymphatic
endothelial
function
to
drive
aberrant
vascularization
in
the
tumour
microenvironment
(TME);
however,
molecular
determinants
govern
functional
role
of
EndoMT
remain
unclear.
Here,
we
show
cancer-associated
fibroblast
(CAF)-derived
PAI-1
promoted
cells
(LECs)
cervical
squamous
cell
carcinoma
(CSCC).Immunofluorescent
staining
α-SMA,
LYVE-1
and
DAPI
were
examined
primary
samples
obtained
from
57
CSCC
patients.
Assessment
cytokines
secreted
by
CAFs
normal
fibroblasts
(NFs)
was
performed
using
human
cytokine
antibody
arrays.
The
phenotype
(LECs),
gene
expression
levels,
protein
secretion
activity
signaling
pathways
measured
real-time
RT-PCR,
ELISA
or
western
blotting.
monolayers
transwell,
tube
formation
assay,
transendothelial
migration
assay
vitro.
Lymphatic
metastasis
popliteal
lymph
node
model.
Furthermore,
association
between
analyzed
immunohistochemistry.
Cancer
Genome
Atlas
(TCGA)
databases
used
assess
with
survival
rate
CSCC.CAF-derived
LECs
CSCC.
undergoing
could
initiate
neolymphangiogenesis
facilitated
cancer
intravasation/extravasation,
which
turn
Mechanistically,
activated
AKT/ERK1/2
directly
interacting
low-density
lipoprotein
receptor-related
(LRP1),
thereby
leading
elevated
LECs.
Blockade
inhibition
LRP1/AKT/ERK1/2
abrogated
consequently
attenuated
CAF-induced
neolymphangiogenesis.
clinical
data
revealed
increased
levels
positively
correlated
poor
prognosis
patients.Our
indicate
CAF-derived
acts
as
important
neolymphangiogenesis-initiating
during
progression
through
modulating
LECs,
resulting
promotion
ability
site.
serve
effective
prognostic
biomarker
therapeutic
target
for
metastasis.
Biochemical Society Transactions,
Journal Year:
2020,
Volume and Issue:
48(3), P. 1187 - 1198
Published: May 15, 2020
The
Wnt/β-catenin
signaling
pathway
plays
fundamental
roles
during
development,
stem
cell
differentiation,
and
homeostasis,
its
abnormal
activation
can
lead
to
diseases.
In
recent
years,
it
has
become
clear
that
this
integrates
signals
not
only
from
Wnt
ligands
but
also
other
proteins
routes.
For
instance,
involves
YAP
TAZ,
which
are
transcription
factors
with
crucial
in
mechanotransduction.
On
the
hand,
is
modulated
by
integrins.
Therefore,
mechanical
might
similarly
modulate
pathway.
However,
despite
relevance
mechanosensitive
have
physiology
diseases
such
as
cancer,
role
of
cues
on
received
less
attention.
This
review
aims
summarize
evidence
regarding
modulation
a
specific
type
signal,
stiffness
extracellular
matrix.
shows
indeed
several
types,
through
differential
expression
ligands,
receptors
inhibitors,
well
modulating
β-catenin
levels.
mechanisms
yet
be
fully
elucidated.
Clinical & Experimental Immunology,
Journal Year:
2021,
Volume and Issue:
205(1), P. 12 - 27
Published: March 27, 2021
Systemic
sclerosis
(SSc)
is
an
autoimmune
disease
characterized
by
significant
vascular
alterations
and
multi-organ
fibrosis.
Microvascular
are
the
first
event
of
SSc
injured
endothelial
cells
(ECs)
may
transdifferentiate
towards
myofibroblasts,
responsible
for
fibrosis
collagen
deposition.
This
process
identified
as
endothelial-to-mesenchymal
transition
(EndMT),
understanding
its
development
pivotal
to
identify
early
pathogenetic
events
new
therapeutic
targets
SSc.
In
this
review,
we
have
highlighted
molecular
mechanisms
EndMT
summarize
evidence
role
played
during
progressive
in
SSc,
also
exploring
possible
inhibition.
