ArticleThe American journal of pathology2010
Inhibition of glycogen synthase kinase 3beta (GSK3beta) decreases inflammatory responses in brain endothelial cells.
Article in The American journal of pathology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 80 citations in OpenAlex.
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- Endothelial cell glycogen synthase kinase 3β promotes lipotoxic endotheliopathy and liver inflammation in MASH.JCI insight · 2026Article
- Physical activity and glioblastoma: a paradigm shift in neuro-oncology therapy.Frontiers in oncology · 2025Review
- Glycogen synthase kinase 3 activity enhances liver inflammation in MASH.JHEP reports : innovation in hepatology · 2024Article
- Genetic and Pharmacological Modulation of P75 Neurotrophin Receptor Attenuate Brain Damage After Ischemic Stroke in Mice.Molecular neurobiology · 2024Article
- Intravital Microscopy of Lipopolysaccharide-Induced Inflammatory Changes in Different Organ Systems-A Scoping Review.International journal of molecular sciences · 2023Article
- The Blood-Brain Barrier: Much More Than a Selective Access to the Brain.Neurotoxicity research · 2021Review
- Real-Time Imaging of Immune Modulation by Cannabinoids Using Intravital Fluorescence Microscopy.Cannabis and cannabinoid research · 2021Review
- Molecular Biology of Atherosclerotic Ischemic Strokes.International journal of molecular sciences · 2020Review
- miR-98 reduces endothelial dysfunction by protecting blood-brain barrier (BBB) and improves neurological outcomes in mouse ischemia/reperfusion stroke model.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2020Article
- In vitro modeling of blood-brain barrier and interface functions in neuroimmune communication.Fluids and barriers of the CNS · 2020Review
- Forkhead box O1 (FOXO1) controls the migratory response of Toll-like receptor (TLR3)-stimulated human mesenchymal stromal cells.The Journal of biological chemistry · 2019Article
- Recent Expansions on Cellular Models to Uncover the Scientific Barriers Towards Drug Development for Alzheimer's Disease.Cellular and molecular neurobiology · 2019Review
- Blood-brain barrier permeability and physical exercise.Journal of neuroinflammation · 2019Review
- A Peptide Targeting Inflammatory CNS Lesions in the EAE Rat Model of Multiple Sclerosis.Inflammation · 2018Article
- Characterization of human fetal brain endothelial cells reveals barrier properties suitable for in vitro modeling of the BBB with syngenic co-cultures.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2018Article
- The deubiquitinating enzyme USP48 stabilizes TRAF2 and reduces E-cadherin-mediated adherens junctions.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018Article
- Potential involvement of glycogen synthase kinase (GSK)-3β in a rat model of multiple sclerosis: evidenced by lithium treatment.Anatomy & cell biology · 2017Article
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Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Immune mediators and leukocyte engagement of brain microvascular endothelial cells (BMVECs) contribute to blood-brain barrier impairment during neuroinflammation. Glycogen synthase kinase 3beta (GSK3beta) was recently identified as a potent regulator of immune responses in in vitro systems and animal models. However, the role of GSK3beta in regulation of immune endothelial functions remains undetermined. Here we evaluated the effect of GSK3beta inhibition on the regulation of inflammatory responses in BMVECs. A focused PCR gene array of 84 genes was performed to identify the cytokine and chemokine gene expression profile in tumor necrosis factor (TNF) alpha-stimulated BMVECs after GSK3beta inactivation by specific inhibitors. Fifteen of 39 genes induced by TNFalpha stimulation were down-regulated after GSK3beta inhibition. Genes known to contribute to neuroinflammation that were most negatively affected by GSK3beta inactivation included IP-10/CXCL10, MCP-1/CCL2, IL-8/CXCL8, RANTES/CCL5, and Groalpha/CXCL1. GSK3beta suppression resulted in diminished secretion of these proinflammatory mediators by inflamed BMVECs detected by ELISA. GSK3beta inhibition in BMVECs reduced adhesion molecule expression as well as monocyte adhesion to and migration across cytokine stimulated BMVEC monolayers. Interactions of monocytes with TNFalpha-activated BMVECs led to barrier disruption, and GSK3beta suppression in the endothelium restored barrier integrity. GSK3beta inhibition in vivo substantially decreased leukocyte adhesion to brain endothelium under inflammatory conditions. In summary, inhibition of GSK3beta emerges as an important target for stabilization of the blood-brain barrier in neuroinflammation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.