Characterization of Mucosal Immune-Related lncRNAs and mRNAs in a Mouse Model of Allergic Conjunctivitis
Hong Zhang,
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Hongyu Zhang,
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Qing Leng
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et al.
Journal of Inflammation Research,
Journal Year:
2025,
Volume and Issue:
Volume 18, P. 6061 - 6076
Published: May 1, 2025
Allergic
conjunctivitis
(AC)
is
a
common
inflammatory
condition
characterized
by
immune
dysregulation
in
response
to
environmental
allergens.
Despite
extensive
research
into
general
allergic
mechanisms,
the
specific
immunological
features
of
ocular
mucosal
microenvironment
remain
poorly
understood.
Investigating
immune-related
mRNAs
and
LncRNAs
may
provide
insights
mechanisms
underlying
AC
potential
novel
targets
for
therapeutic
intervention.
An
model
was
established
using
female
BALB/c
mice
sensitized
with
ragweed
pollen.
Conjunctival
tissues
from
control
groups
were
pooled
RNA
extraction,
followed
Illumina
sequencing.
Differential
gene
expression
identified
DESeq2,
functional
enrichment
analyzed
GO,
KEGG,
GSEA.
RT-qPCR
validated
results,
while
Human
Protein
Atlas
used
assess
protein
expression.
A
murine
successfully
established,
confirmed
progressively
increasing
clinical
scores
significantly
elevated
scratching
frequency.
Transcriptomic
analysis
revealed
significant
differences
lncRNAs
between
groups.
GO
indicated
that
both
upregulated
downregulated
genes
enriched
biological
processes
related
stimulus,
system
processes,
signaling,
metabolic
processes.
KEGG
showed
pathways
such
as
steroid
hormone
biosynthesis,
histidine
metabolism,
glycolysis/gluconeogenesis,
IL-17
involved
cytokine-cytokine
receptor
interaction
hematopoietic
cell
lineage.
GSEA
pathways,
including
MAPK,
STAT1,
STAT2.
Mucosal
immunity-related
Bpifa1,
Lcn2,
Reg3g
AC.
Co-expression
also
several
lncRNAs,
Stoml3-202
Etohd2-205.
This
study
first
systematically
analyze
AC,
identifying
immunity
molecules
like
Bpifa1
Reg3g.
These
findings
underscore
unique
involvement
new
modulation
allergy
treatment.
Language: Английский
Autophagy Impairment-Derived SQSTM1 Accumulation Promotes Ferroptosis in Corneal Epithelial Cells Through ACSL4 in Dry Eye
Investigative Ophthalmology & Visual Science,
Journal Year:
2025,
Volume and Issue:
66(5), P. 23 - 23
Published: May 13, 2025
To
reveal
the
function
of
autophagy
impairment-derived
sequestosome
1
(SQSTM1)
in
inducing
ferroptosis
an
experimental
dry
eye
model
and
investigate
underlying
mechanism.
induce
animal
model,
8-week-old
C57BL/6
mice
were
subcutaneously
injected
with
scopolamine
exposed
to
a
desiccated
environment.
build
vitro
human
corneal
epithelial
cells
(HCECs)
applied
desiccating
stress.
Cell
viability
was
examined
using
CCK-8
kit.
Intracellular
reactive
oxygen
species
(ROS),
oxidative
lipid,
Fe2+
detected
H2DCFDA
assay
kit,
C11
BODIPY
probe,
FerroOrange
probe.
Gene
expression
screened
by
RNA
sequencing.
Protein
evaluated
western
blot
immunofluorescence
staining.
Corneal
defect
area
assessed
fluorescein
sodium
Conjunctiva
goblet
counted
periodic
acid-Schiff
Tear
secretion
measured
phenol
red
cotton
thread.
Desiccating
stress
induced
SQSTM1
accumulation
both
HCECs
mice.
knockdown
alleviated
HCECs.
In
contrast,
overexpression
promoted
ferroptotic
changes.
Additionally,
significantly
increased
acyl-CoA
synthetase
long
chain
family
member
4
(ACSL4).
Also,
targeted
inhibition
ACSL4
mitigated
symptoms
caused
The
triggers
through
disease.
Language: Английский