Cited by 242Neuroinflammation and Neurodegeneration MechanismsNeuroscience and Neuropharmacology ResearchPain Mechanisms and Treatments

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Glycogen synthase kinase-3 regulates microglial migration, inflammation, and inflammation-induced neurotoxicity

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Yuskaitis, Christopher J., Jope, Richard S.·2009·Cellular Signalling

DOI 10.1016/j.cellsig.2008.10.014PMC PMC2630396

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Abstract

Microglia play a prominent role in the brain's inflammatory response to injury or infection by migrating to affected locations, secreting inflammatory molecules, and phagocytosing damaged tissue. However, because severe or chronic neuroinflammation exacerbates many neurological conditions, controlling microglia actions may provide therapeutic benefits in a diverse array of diseases. Since glycogen synthase kinase-3 (GSK3) promotes inflammatory responses in peripheral immune cells, we investigated if inhibitors of GSK3 attenuated microglia responses to inflammatory stimuli. Treatment of BV-2 microglia with GSK3 inhibitors greatly reduced the migration of microglia in both a scratch assay and in a transwell migration assay. Treatment of BV-2 microglia with lipopolysaccharide (LPS) stimulated the production of interleukin-6 and increased the expression of inducible nitric oxide synthase (iNOS) and NO production. Each of these microglia responses to inflammatory stimulation were greatly attenuated by GSK3 inhibitors. However, GSK3 inhibitors did not cause a general impairment of microglia functions, as the LPS-induced stimulated expression of cyclooxygenase-2 was unaltered. Regulation of microglia functions were also evident in cultured mouse hippocampal slices where GSK3 inhibitors reduced cytokine production and microglial migration, and provided protection from inflammation-induced neuronal toxicity. These findings demonstrate that GSK3 promotes microglial responses to inflammation and that the utilization of GSK3 inhibitors provides a means to limit the inflammatory actions of microglia.

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“…found that audiogenic seizures, open field testing and cerebral protein synthesis phenotypes can be reliably obtained and rescued by lithium or GSK3B inhibition (Min et al., 2009a; Yuskaitis and Jope, 2009; Mines et al., 2010; Yuskaitis et al., 2010; Liu et al., 2011, 2012; Mines and Jope, 2011).”
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Background
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“Previous studies have shown that activation of MAPKs, PI3K/ Akt, and GSK-3β has a significant effect on iNOS, COX-2, and pro-inflammatory cytokine gene expression in microglia by controlling the activation of NF-κB (Surh et al., 2001; Li et al., 2006; Yuskaitis and Jope, 2009).”
Background
Staphylococcus aureusInduces Microglial Inflammation via a Glycogen Synthase Kinase 3β-Regulated Pathway
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BackgroundInfluential
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Anti-Inflammatory Activity and Structure-Activity Relationships of Brominated Indoles from a Marine Mollusc
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“This result was unexpected given that indirubin is known to inhibit glycogen synthase kinase-3 (GSK3) [45], which promotes anti-inflammatory responses, including LPS induced NO production [46].”
Background

Authors: Yuskaitis, C. J., & Jope, R. S.
Affiliations: University of Alabama at Birmingham (US)
Corresponding author: Jope, Richard S.
ORCID: Yuskaitis, Christopher J.
Venue: Cellular Signalling
Publisher: Elsevier BV
Published: 2009-02
Volume: 21
Issue: 2
Pages: 264-273
ISSN: 0898-6568 (ISSN-L)
DOI: 10.1016/j.cellsig.2008.10.014
PMC: PMC2630396
OpenAlex: W2054780831
Cited by: 240
References: 66
Citations by year: 2026: 7 · 2025: 14 · 2024: 15 · 2023: 11 · 2022: 15 · 2021: 17 · 2020: 13 · 2019: 12 · 2018: 18 · 2017: 9 · 2016: 18 · 2015: 7 · 2014: 24 · 2013: 16 · 2012: 14
FWCI: 6.56
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/legal/tdmrep-license (tdm)
doi.org/10.15223/policy-017 (stm-asf)
doi.org/10.15223/policy-037 (stm-asf)
doi.org/10.15223/policy-012 (stm-asf)
doi.org/10.15223/policy-029 (stm-asf)
doi.org/10.15223/policy-004 (stm-asf)
Locations: Cellular Signalling (publishedVersion)
PubMed (publishedVersion)
Europe PMC (PubMed Central) (acceptedVersion)
PubMed Central (acceptedVersion)
Funders: University of Dundee
National Institute on Aging (AG021045, R01AG021045)
National Institute of Mental Health (MH38752, R56MH038752, R01MH038752)
National Institute of Neurological Disorders and Stroke (NS47466, P30NS047466, R01NS037768, P30NS057098, NS3768, NS57098)
Topics: Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
Health Sciences › Medicine › Physiology (medical) › Pain Mechanisms and Treatments
Keywords: glycogen synthase kinase-3, GSK-3 inhibitors, microglia, microglial migration, neuroinflammation, lipopolysaccharide, interleukin-6, inducible nitric oxide synthase, nitric oxide, cyclooxygenase-2, hippocampus, BV-2 cells
MeSH terms: Animals, Benzazepines, Cell Movement, Cells, Cultured, Indoles, Lipopolysaccharides, Lithium, Nitric Oxide, Oximes, Interleukin-6, Microglia, Inflammation Mediators, Nitric Oxide Synthase, Glycogen Synthase Kinase 3, Mice

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Glycogen synthase kinase-3 regulates microglial migration, inflammation, and inflammation-induced neurotoxicity

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