Redox Biology,
Год журнала:
2023,
Номер
60, С. 102618 - 102618
Опубликована: Янв. 28, 2023
The
intestinal
epithelial
repair
after
injury
is
coordinated
by
stem
cells
(ISCs).
Fucosylation
catalyzed
fucosyltransferase
2
(FUT2)
of
the
epithelium
beneficial
to
mucosal
healing
but
poorly
defined
influence
on
ISCs.
dextran
sulfate
sodium
(DSS)
and
lipopolysaccharide
(LPS)
model
were
used
assess
role
FUT2
ISCs
injury.
apoptosis,
function,
stemness
analyzed
using
organoids
from
WT
Fut2ΔISC
(ISC-specific
Fut2
knockout)
mice
incubated
with
LPS
fucose.
N-glycoproteomics,
UEA-1
chromatography,
site-directed
mutagenesis
monitored
dissect
regulatory
mechanism,
identify
target
fucosylated
protein
corresponding
modification
site.
Fucose
could
alleviate
damage
via
upregulating
α-1,2-fucosylation
Oxidative
stress,
mitochondrial
dysfunction,
cell
apoptosis
impeded
Meanwhile,
fucose
sustained
growth
proliferation
capacity
treated
LPS.
Contrarily,
depletion
in
aggravated
disrupted
escalating
LPS-induced
endoplasmic
reticulum
(ER)
stress
initiating
IRE1/TRAF2/ASK1/JNK
branch
unfolded
response
(UPR).
chaperone
HYOU1
at
N-glycosylation
site
asparagine
(Asn)
862
mediated
was
identified
facilitate
survival
self-renewal,
improve
resistance
ER
inflammatory
Our
study
highlights
a
fucosylation-dependent
protective
mechanism
against
inflammation,
which
may
provide
fascinating
strategy
for
treating
disorders.
The
endoplasmic
reticulum
(ER)
mediates
the
first
steps
of
protein
assembly
within
secretory
pathway
and
is
site
where
folding
quality
control
are
initiated.
storage
release
Ca2+
critical
physiological
functions
ER.
Disrupted
ER
homeostasis
activates
unfolded
response
(UPR),
a
which
attempts
to
restore
cellular
equilibrium
in
face
stress.
Unremitting
stress,
insufficient
compensation
for
it
results
beta-cell
apoptosis,
process
that
has
been
linked
both
type
1
diabetes
(T1D)
2
(T2D).
Both
types
characterized
by
progressive
failure
loss
mass,
although
underlying
causes
different.
reduction
mass
occurs
secondary
apoptosis
case
T2D,
while
beta
cells
undergo
autoimmune
destruction
T1D.
In
this
review,
we
examine
recent
findings
link
UPR
cell
dysfunction.
We
also
discuss
how
activation
favors
survival
versus
death,
chaperones
involved
regulating
levels.
Abbreviations:
BiP,
Binding
immunoglobulin
Protein
ER;
reticulum;
ERAD,
ER-associated
degradation;
IFN,
interferon;
IL,
interleukin;
JNK,
c-Jun
N-terminal
kinase;
KHE,
proton-K+
exchanger;
MODY,
maturity-onset
young;
PERK,
PRKR-like
SERCA,
Sarco/Endoplasmic
Reticulum
Ca2+-ATPases;
T1D,
diabetes;
TNF,
tumor
necrosis
factor;
UPR,
response;
WRS,
Wolcott-Rallison
syndrome.
Science Signaling,
Год журнала:
2022,
Номер
15(741)
Опубликована: Июль 5, 2022
The
endoplasmic
reticulum
(ER)
is
the
largest
organelle
of
cell
and
participates
in
multiple
essential
functions,
including
production
secretory
proteins,
lipid
synthesis,
calcium
storage.
Sustaining
proteostasis
requires
an
intimate
coupling
with
energy
production.
Mitochondrial
respiration
evolved
to
be
functionally
connected
ER
physiology
through
a
physical
interface
between
both
organelles
known
as
mitochondria-associated
membranes.
This
quasi-synaptic
structure
acts
signaling
hub
that
tunes
function
bidirectional
manner
controls
proteostasis,
death
pathways,
mitochondrial
bioenergetics.
Here,
we
discuss
main
mechanisms
governing
interorganellar
communication
their
putative
role
diseases
cancer
neurodegeneration.
Redox Biology,
Год журнала:
2023,
Номер
60, С. 102618 - 102618
Опубликована: Янв. 28, 2023
The
intestinal
epithelial
repair
after
injury
is
coordinated
by
stem
cells
(ISCs).
Fucosylation
catalyzed
fucosyltransferase
2
(FUT2)
of
the
epithelium
beneficial
to
mucosal
healing
but
poorly
defined
influence
on
ISCs.
dextran
sulfate
sodium
(DSS)
and
lipopolysaccharide
(LPS)
model
were
used
assess
role
FUT2
ISCs
injury.
apoptosis,
function,
stemness
analyzed
using
organoids
from
WT
Fut2ΔISC
(ISC-specific
Fut2
knockout)
mice
incubated
with
LPS
fucose.
N-glycoproteomics,
UEA-1
chromatography,
site-directed
mutagenesis
monitored
dissect
regulatory
mechanism,
identify
target
fucosylated
protein
corresponding
modification
site.
Fucose
could
alleviate
damage
via
upregulating
α-1,2-fucosylation
Oxidative
stress,
mitochondrial
dysfunction,
cell
apoptosis
impeded
Meanwhile,
fucose
sustained
growth
proliferation
capacity
treated
LPS.
Contrarily,
depletion
in
aggravated
disrupted
escalating
LPS-induced
endoplasmic
reticulum
(ER)
stress
initiating
IRE1/TRAF2/ASK1/JNK
branch
unfolded
response
(UPR).
chaperone
HYOU1
at
N-glycosylation
site
asparagine
(Asn)
862
mediated
was
identified
facilitate
survival
self-renewal,
improve
resistance
ER
inflammatory
Our
study
highlights
a
fucosylation-dependent
protective
mechanism
against
inflammation,
which
may
provide
fascinating
strategy
for
treating
disorders.
