Removal of IKK in microglia induces changes in microglia number and morphology during prion infection.

<p>Terminal mice with IKK KO microglia were compared to wpi-matched WT infected mice. <b>A</b> Brains were stained for Iba1 + microglia, which were counted and compared in the <b>B</b> cortex, <b>C</b> hippocampus, <b>D</b> thalamus and <b>...

Cur síos iomlán

Sábháilte in:
Sonraí bibleagrafaíochta
Príomhchruthaitheoir: Arielle J. D. Hay (15456341) (author)
Rannpháirtithe: Katriana A. Popichak (12093647) (author), Genova Mumford (15456344) (author), Jifeng Bian (354060) (author), Payton Shirley (21568259) (author), Lauren Wolfrath (21568262) (author), Michael Eggers (21568265) (author), Eric M. Nicholson (8262054) (author), Ronald B. Tjalkens (3281031) (author), Mark D. Zabel (15456359) (author), Julie A. Moreno (7647266) (author)
Foilsithe / Cruthaithe: 2025
Ábhair:
Clibeanna: Cuir clib leis
Níl clibeanna ann, Bí ar an gcéad duine le clib a chur leis an taifead seo!
_version_ 1851485295521824768
author Arielle J. D. Hay (15456341)
author2 Katriana A. Popichak (12093647)
Genova Mumford (15456344)
Jifeng Bian (354060)
Payton Shirley (21568259)
Lauren Wolfrath (21568262)
Michael Eggers (21568265)
Eric M. Nicholson (8262054)
Ronald B. Tjalkens (3281031)
Mark D. Zabel (15456359)
Julie A. Moreno (7647266)
author2_role author
author
author
author
author
author
author
author
author
author
author_facet Arielle J. D. Hay (15456341)
Katriana A. Popichak (12093647)
Genova Mumford (15456344)
Jifeng Bian (354060)
Payton Shirley (21568259)
Lauren Wolfrath (21568262)
Michael Eggers (21568265)
Eric M. Nicholson (8262054)
Ronald B. Tjalkens (3281031)
Mark D. Zabel (15456359)
Julie A. Moreno (7647266)
author_role author
dc.creator.none.fl_str_mv Arielle J. D. Hay (15456341)
Katriana A. Popichak (12093647)
Genova Mumford (15456344)
Jifeng Bian (354060)
Payton Shirley (21568259)
Lauren Wolfrath (21568262)
Michael Eggers (21568265)
Eric M. Nicholson (8262054)
Ronald B. Tjalkens (3281031)
Mark D. Zabel (15456359)
Julie A. Moreno (7647266)
dc.date.none.fl_str_mv 2025-06-18T17:58:53Z
dc.identifier.none.fl_str_mv 10.1371/journal.ppat.1012582.g003
dc.relation.none.fl_str_mv https://figshare.com/articles/figure/Removal_of_IKK_in_microglia_induces_changes_in_microglia_number_and_morphology_during_prion_infection_/29360291
dc.rights.none.fl_str_mv CC BY 4.0
info:eu-repo/semantics/openAccess
dc.subject.none.fl_str_mv Medicine
Microbiology
Cell Biology
Genetics
Molecular Biology
Neuroscience
Physiology
Immunology
Cancer
Infectious Diseases
iκb kinase complex
cellular stress signals
irreversible neuronal loss
associated behavioral deficits
sc </ sup
prion disease pathogenesis
prion disease early
div >< p
cellular prion protein
inflammatory signaling molecules
infected brain homogenates
terminal wt mice
induced glial inflammation
accelerated disease
terminal animals
protein homeostasis
inflammatory cytokines
induced transcription
accelerated loss
prion diseases
signaling pathway
intracranially infected
infected wild
infected brain
b signaling
specific pathology
significantly lower
significantly increased
significantly downregulated
poorly understood
nuclear factor
near ablation
microglial survival
key regulator
kappa b
infectious form
increased density
including pro
host protection
hippocampal neurons
glial cells
forms aggregates
findings present
cell survival
associated genes
dc.title.none.fl_str_mv Removal of IKK in microglia induces changes in microglia number and morphology during prion infection.
dc.type.none.fl_str_mv Image
Figure
info:eu-repo/semantics/publishedVersion
image
description <p>Terminal mice with IKK KO microglia were compared to wpi-matched WT infected mice. <b>A</b> Brains were stained for Iba1 + microglia, which were counted and compared in the <b>B</b> cortex, <b>C</b> hippocampus, <b>D</b> thalamus and <b>E</b> cerebellum for 9 animals with IKK KO microglia, 6 wpi-matched WT and 3 terminal WT animals. Scale bars = 20·m. <b>F</b> Representative images of Iba1 + hippocampal microglia morphological skeletons between groups. Scale bar = 10·m. <b>G</b> Microglia cartoon depicting features analyzed via skeletonization, created with Biorender.com. <b>H</b> Process length, <b>I</b> number of process branches and <b>J</b> number of process endpoints was compared between hippocampal microglia from WT mice and those with IKK KO microglia. Skeletonization and C3 analysis were performed on 3 randomly selected animals per group. Welch’s t-test, error bars = SEM, **<i>p</i> < 0.01, ****<i>p </i>< 0.0001.</p>
eu_rights_str_mv openAccess
id Manara_c418b0b0197fd6a673ee65bcffc065e7
identifier_str_mv 10.1371/journal.ppat.1012582.g003
network_acronym_str Manara
network_name_str ManaraRepo
oai_identifier_str oai:figshare.com:article/29360291
publishDate 2025
repository.mail.fl_str_mv
repository.name.fl_str_mv
repository_id_str
rights_invalid_str_mv CC BY 4.0
spelling Removal of IKK in microglia induces changes in microglia number and morphology during prion infection.Arielle J. D. Hay (15456341)Katriana A. Popichak (12093647)Genova Mumford (15456344)Jifeng Bian (354060)Payton Shirley (21568259)Lauren Wolfrath (21568262)Michael Eggers (21568265)Eric M. Nicholson (8262054)Ronald B. Tjalkens (3281031)Mark D. Zabel (15456359)Julie A. Moreno (7647266)MedicineMicrobiologyCell BiologyGeneticsMolecular BiologyNeurosciencePhysiologyImmunologyCancerInfectious Diseasesiκb kinase complexcellular stress signalsirreversible neuronal lossassociated behavioral deficitssc </ supprion disease pathogenesisprion disease earlydiv >< pcellular prion proteininflammatory signaling moleculesinfected brain homogenatesterminal wt miceinduced glial inflammationaccelerated diseaseterminal animalsprotein homeostasisinflammatory cytokinesinduced transcriptionaccelerated lossprion diseasessignaling pathwayintracranially infectedinfected wildinfected brainb signalingspecific pathologysignificantly lowersignificantly increasedsignificantly downregulatedpoorly understoodnuclear factornear ablationmicroglial survivalkey regulatorkappa binfectious formincreased densityincluding prohost protectionhippocampal neuronsglial cellsforms aggregatesfindings presentcell survivalassociated genes<p>Terminal mice with IKK KO microglia were compared to wpi-matched WT infected mice. <b>A</b> Brains were stained for Iba1 + microglia, which were counted and compared in the <b>B</b> cortex, <b>C</b> hippocampus, <b>D</b> thalamus and <b>E</b> cerebellum for 9 animals with IKK KO microglia, 6 wpi-matched WT and 3 terminal WT animals. Scale bars = 20·m. <b>F</b> Representative images of Iba1 + hippocampal microglia morphological skeletons between groups. Scale bar = 10·m. <b>G</b> Microglia cartoon depicting features analyzed via skeletonization, created with Biorender.com. <b>H</b> Process length, <b>I</b> number of process branches and <b>J</b> number of process endpoints was compared between hippocampal microglia from WT mice and those with IKK KO microglia. Skeletonization and C3 analysis were performed on 3 randomly selected animals per group. Welch’s t-test, error bars = SEM, **<i>p</i> < 0.01, ****<i>p </i>< 0.0001.</p>2025-06-18T17:58:53ZImageFigureinfo:eu-repo/semantics/publishedVersionimage10.1371/journal.ppat.1012582.g003https://figshare.com/articles/figure/Removal_of_IKK_in_microglia_induces_changes_in_microglia_number_and_morphology_during_prion_infection_/29360291CC BY 4.0info:eu-repo/semantics/openAccessoai:figshare.com:article/293602912025-06-18T17:58:53Z
spellingShingle Removal of IKK in microglia induces changes in microglia number and morphology during prion infection.
Arielle J. D. Hay (15456341)
Medicine
Microbiology
Cell Biology
Genetics
Molecular Biology
Neuroscience
Physiology
Immunology
Cancer
Infectious Diseases
iκb kinase complex
cellular stress signals
irreversible neuronal loss
associated behavioral deficits
sc </ sup
prion disease pathogenesis
prion disease early
div >< p
cellular prion protein
inflammatory signaling molecules
infected brain homogenates
terminal wt mice
induced glial inflammation
accelerated disease
terminal animals
protein homeostasis
inflammatory cytokines
induced transcription
accelerated loss
prion diseases
signaling pathway
intracranially infected
infected wild
infected brain
b signaling
specific pathology
significantly lower
significantly increased
significantly downregulated
poorly understood
nuclear factor
near ablation
microglial survival
key regulator
kappa b
infectious form
increased density
including pro
host protection
hippocampal neurons
glial cells
forms aggregates
findings present
cell survival
associated genes
status_str publishedVersion
title Removal of IKK in microglia induces changes in microglia number and morphology during prion infection.
title_full Removal of IKK in microglia induces changes in microglia number and morphology during prion infection.
title_fullStr Removal of IKK in microglia induces changes in microglia number and morphology during prion infection.
title_full_unstemmed Removal of IKK in microglia induces changes in microglia number and morphology during prion infection.
title_short Removal of IKK in microglia induces changes in microglia number and morphology during prion infection.
title_sort Removal of IKK in microglia induces changes in microglia number and morphology during prion infection.
topic Medicine
Microbiology
Cell Biology
Genetics
Molecular Biology
Neuroscience
Physiology
Immunology
Cancer
Infectious Diseases
iκb kinase complex
cellular stress signals
irreversible neuronal loss
associated behavioral deficits
sc </ sup
prion disease pathogenesis
prion disease early
div >< p
cellular prion protein
inflammatory signaling molecules
infected brain homogenates
terminal wt mice
induced glial inflammation
accelerated disease
terminal animals
protein homeostasis
inflammatory cytokines
induced transcription
accelerated loss
prion diseases
signaling pathway
intracranially infected
infected wild
infected brain
b signaling
specific pathology
significantly lower
significantly increased
significantly downregulated
poorly understood
nuclear factor
near ablation
microglial survival
key regulator
kappa b
infectious form
increased density
including pro
host protection
hippocampal neurons
glial cells
forms aggregates
findings present
cell survival
associated genes