PLoS Biology,
Journal Year:
2024,
Volume and Issue:
22(6), P. e3002662 - e3002662
Published: June 13, 2024
The
polygonal
shape
of
cells
in
proliferating
epithelia
is
a
result
the
tensile
forces
cytoskeletal
cortex
and
packing
geometry
set
by
cell
cycle.
In
larval
Drosophila
epidermis,
two
populations,
histoblasts
epithelial
cells,
compete
for
space
as
they
grow
on
limited
body
surface.
They
do
so
absence
divisions.
We
report
striking
morphological
transition
during
development,
where
change
from
tensed
network
configuration
with
straight
outlines
at
level
adherens
junctions
to
highly
folded
morphology.
apical
surface
shrinks
while
their
growing
fold,
forming
deep
lobules.
Volume
increase
accommodated
basally,
compensating
shrinking
area.
resembles
elastic
buckling,
we
show
that
imbalance
between
shrinkage
domain
continuous
growth
triggers
buckling.
Our
model
supported
laser
dissections
optical
tweezer
experiments
together
computer
simulations.
analysis
pinpoints
ability
store
mechanical
energy
much
greater
extent
than
most
other
types
investigated
far,
retaining
dissipate
stress
hours
time
scale.
Finally,
propose
possible
mechanism
size
regulation
histoblast
through
lateral
pressure
driven
Buckling
effectively
compacts
plane
may
serve
avoid
physical
harm
these
adult
epidermis
precursors
life.
work
indicates
nondividing
compressive
forces,
instead
tension,
drive
Pharmaceutics,
Journal Year:
2019,
Volume and Issue:
11(3), P. 129 - 129
Published: March 19, 2019
Routes
of
drug
administration
and
the
corresponding
physicochemical
characteristics
a
given
route
play
significant
roles
in
therapeutic
efficacy
short
term/long
term
biological
effects.
Each
delivery
method
has
favorable
aspects
limitations,
each
requiring
specific
vehicles
design.
Among
various
routes,
oral
been
recognized
as
most
attractive
method,
mainly
due
to
its
potential
for
solid
formulations
with
long
shelf
life,
sustained
delivery,
ease
intensified
immune
response.
At
same
time,
few
challenges
exist
which
have
main
research
focus
field
past
years.
The
present
work
concisely
reviews
different
routes
well
advantages
disadvantages
highlighting
why
is
currently
promising
approach.
Subsequently,
discusses
obstacles
systems
explains
recent
solutions
proposed
deal
issue.
Seminars in Cancer Biology,
Journal Year:
2019,
Volume and Issue:
63, P. 69 - 80
Published: May 9, 2019
The
regulation
of
cell
growth,
proliferation
and
death
is
at
the
basis
homeostasis
tissues.
While
they
can
be
regulated
by
intrinsic
genetic
factors,
their
response
to
external
signals
emanating
from
local
environment
also
essential
for
tissue
homeostasis.
Tumour
initiation
progression
based
on
misregulation
mostly
through
accumulation
mutations.
Yet,
there
an
increasing
body
evidences
showing
that
tumour
microenvironment
has
a
strong
impact
cancer
progression.
This
includes
mechanical
constrains
compressive
forces
generated
resistance
surrounding
tissue/matrix
expansion.
Recently,
stress
been
proposed
promote
competitive
interactions
between
cells
process
called
competition.
Cell
population
with
high
proliferative
rate
compact
eliminate
neighbouring
which
are
more
sensitive
compaction.
this
emerging
concept
recently
validated
in
vivo,
relevance
during
never
discussed
extensively.
In
review,
I
will
first
describe
phenomenology
competition
focusing
main
parameters
pathways
regulating
elimination.
then
discuss
expansion
while
emphasizing
its
potential
opposing
contributions
tumourogenesis.
Current Biology,
Journal Year:
2019,
Volume and Issue:
29(15), P. R762 - R774
Published: Aug. 1, 2019
Cell
competition
is
a
widespread
process
leading
to
the
expansion
of
one
cell
population
through
elimination
and
replacement
another.
A
large
number
genetic
alterations
can
lead
either
competitive
mutated
or
cells
neighbouring
cells.
Several
processes
have
been
proposed
participate
in
preferential
population,
including
for
limiting
extracellular
pro-survival
factors,
communication
direct
cell–cell
contact,
differential
sensitivity
mechanical
stress.
Recent
quantitative
studies
also
demonstrated
strong
impact
shape
interfaces
between
two
populations.
Here,
we
discuss
indirect
contribution
cues
competition,
where
they
act
as
modulators
interactions
drivers
elimination.
We
first
how
mechanics
regulate
contact-dependent
diffusion-based
by
modulating
interface
then
describe
stress
space.
Finally,
feedback
influences
compensatory
growth
triggers
population.
Regenerative Biomaterials,
Journal Year:
2024,
Volume and Issue:
11
Published: Jan. 1, 2024
Abstract
Increasing
studies
have
revealed
the
importance
of
mechanical
cues
in
tumor
progression,
invasiveness
and
drug
resistance.
During
malignant
transformation,
changes
manifest
either
properties
tissue
or
cellular
ability
to
sense
respond
signals.
The
major
focus
review
is
subtle
correlation
between
apoptosis
cells
from
a
mechanobiology
perspective.
To
begin,
we
on
intracellular
force,
examining
cell
interior,
outlining
role
that
cytoskeleton
organelle-mediated
forces
play
apoptosis.
This
article
also
elucidates
mechanisms
by
which
extracellular
guide
mechanosensing,
ultimately
triggering
activation
mechanotransduction
pathway
impacting
Finally,
comprehensive
examination
present
status
design
development
anti-cancer
materials
targeting
presented,
emphasizing
underlying
principles.
Furthermore,
underscores
need
address
several
unresolved
inquiries
enhance
our
comprehension
cancer
therapeutics
target
mechanotransduction.
Cellular and Molecular Life Sciences,
Journal Year:
2023,
Volume and Issue:
80(12)
Published: Nov. 10, 2023
The
coupling
between
mechanical
forces
and
modulation
of
cell
signalling
pathways
is
essential
for
tissue
plasticity
their
adaptation
to
changing
environments.
Whilst
the
number
physiological
pathological
relevant
roles
mechanotransduction
has
been
rapidly
expanding
over
last
decade,
studies
have
mostly
focussing
on
a
limited
mechanosensitive
pathways,
which
include
instance
Hippo/YAP/TAZ
pathway,
Wnt/β-catenin
or
stretch-activated
channel
Piezo.
However,
recent
development
spreading
new
live
sensors
provided
insights
into
contribution
ERK
pathway
in
mechanosensing
various
systems,
emerges
now
as
fast
modular
pathway.
In
this
review,
we
will
document
key
vivo
vitro
examples
that
established
clear
link
deformation,
stress
signalling,
comparing
timescale
stress.
We
then
discuss
different
molecular
mechanisms
proposed
so
far,
epistatic
mechanics
discussing
cellular
parameters
affecting
signalling.
finish
by
consequences
mechanics,
outlining
how
interplay
instrumental
self-organisation
long-range
cell-cell
coordination.
Development,
Journal Year:
2024,
Volume and Issue:
151(1)
Published: Jan. 1, 2024
ABSTRACT
Cell
junctions
play
key
roles
in
epithelial
integrity.
During
development,
when
epithelia
undergo
extensive
morphogenesis,
these
must
be
remodeled
order
to
maintain
mechanochemical
barriers
and
ensure
the
cohesion
of
tissue.
In
this
Review,
we
present
a
comprehensive
integrated
description
junctional
remodeling
mechanisms
cells
during
from
embryonic
adult
epithelia.
We
largely
focus
on
Drosophila,
as
quantitative
analyses
organism
have
provided
detailed
characterization
molecular
governing
cell
topologies,
discuss
conservation
across
metazoans.
consider
how
changes
at
level
translate
tissue-scale
irreversible
deformations,
exploring
composition
assembly
cellular
interfaces
unveil
are
preserve
tissue
homeostasis
division,
intercalation,
invagination,
ingression
extrusion.
The Journal of Experimental Medicine,
Journal Year:
2021,
Volume and Issue:
219(1)
Published: Dec. 14, 2021
Pathogen-
and
damage-associated
molecular
patterns
are
sensed
by
the
immune
system’s
pattern
recognition
receptors
(PRRs)
upon
contact
with
a
microbe
or
damaged
tissue.
In
situations
such
as
commensals
during
physiological
cell
death,
system
should
not
respond
to
these
patterns.
Hence,
responses
need
be
context
dependent,
but
it
is
clear
how
for
provided.
We
discuss
inhibitory
potential
counterparts
activating
receptors.
propose
group
of
(iPRRs)
that
recognize
endogenous
microbial
associated
danger,
homeostasis,
both.
iPRRs
provides
context,
helps
mediate
tolerance
microbes,
balance
danger
signals.
