ArticleScientific reports2016
Th1 cells downregulate connexin 43 gap junctions in astrocytes via microglial activation.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 48 citations in OpenAlex.
- Interleukin-1β Drives Disease Progression in Arrhythmogenic Cardiomyopathy.JACC. Basic to translational science · 2026Article
- Multiple system atrophy: advances in pathogenesis and emerging therapeutic strategies.Journal of neurology · 2025Review
- Investigation of the Expression, Localization, and Acidosis-Associated Conformational Changes in Connexin 43 in Traumatic Brain Injury with the Development of a Neural Network Model for Assessing Systemic Inflammation.International journal of molecular sciences · 2025Article
- Mechanisms of Action of Propofol in Modulating Microglial Activation in Ischemic Stroke.Molecules (Basel, Switzerland) · 2025Review
- Acupuncture regulates astrocyte neurotoxic polarization to protect blood-brain barrier integrity in delayed thrombolysis through mediating ERK1/2/Cx43 axis.IBRO neuroscience reports · 2025Article
- Interleukin-1β Drives Disease Progression in Arrhythmogenic Cardiomyopathy.bioRxiv : the preprint server for biology · 2024Article
- Glial Cells as Key Regulators in Neuroinflammatory Mechanisms Associated with Multiple Sclerosis.International journal of molecular sciences · 2024Review
- Astroglial connexin 43 is a novel therapeutic target for chronic multiple sclerosis model.Scientific reports · 2024Article
- Article
- The Plasticity of Immune Cell Response Complicates Dissecting the Underlying Pathology of Multiple Sclerosis.Journal of immunology research · 2024Review
- Connexins Control Glial Inflammation in Various Neurological Diseases.International journal of molecular sciences · 2023Review
- Article
- Early and extensive alterations of glial connexins, distal oligodendrogliopathy type demyelination, and nodal/paranodal pathology are characteristic of multiple system atrophy.Brain pathology (Zurich, Switzerland) · 2023Article
- Connexin 43: An Interface Connecting Neuroinflammation to Depression.Molecules (Basel, Switzerland) · 2023Review
- New models of Parkinson's like neuroinflammation in human microglia clone 3: Activation profiles induced by INF-γ plus high glucose and mitochondrial inhibitors.Frontiers in cellular neuroscience · 2022Article
- The circadian rhythms regulated by Cx43-signaling in the pathogenesis of Neuromyelitis Optica.Frontiers in immunology · 2022Article
- Exploration on neurobiological mechanisms of the central-peripheral-central closed-loop rehabilitation.Frontiers in cellular neuroscience · 2022Review
- Astrocytes and Inflammatory T Helper Cells: A Dangerous Liaison in Multiple Sclerosis.Frontiers in immunology · 2022Review
- Dysregulation of Blood-Brain Barrier and Exacerbated Inflammatory Response in Cx47-Deficient Mice after Induction of EAE.Pharmaceuticals (Basel, Switzerland) · 2021Article
- Brain gray matter astroglia-specific connexin 43 ablation attenuates spinal cord inflammatory demyelination.Journal of neuroinflammation · 2021Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We previously reported early and extensive loss of astrocytic connexin 43 (Cx43) in acute demyelinating lesions of multiple sclerosis (MS) patients. Because it is widely accepted that autoimmune T cells initiate MS lesions, we hypothesized that infiltrating T cells affect Cx43 expression in astrocytes, which contributes to MS lesion formation. Primary mixed glial cell cultures were prepared from newborn mouse brains, and microglia were isolated by anti-CD11b antibody-conjugated magnetic beads. Next, we prepared astrocyte-rich cultures and astrocyte/microglia-mixed cultures. Treatment of primary mixed glial cell cultures with interferon (IFN) γ, interleukin (IL)-4, or IL-17 showed that only IFNγ or IL-17 at high concentrations reduced Cx43 protein levels. Upon treatment of astrocyte-rich cultures and astrocyte/microglia-mixed cultures with IFNγ, Cx43 mRNA/protein levels and the function of gap junctions were reduced only in astrocyte/microglia-mixed cultures. IFNγ-treated microglia-conditioned media and IL-1β, which was markedly increased in IFNγ-treated microglia-conditioned media, reduced Cx43 protein levels in astrocyte-rich cultures. Finally, we confirmed that Th1 cell-conditioned medium decreased Cx43 protein levels in mixed glial cell cultures. These findings suggest that Th1 cell-derived IFNγ activates microglia to release IL-1β that reduces Cx43 gap junctions in astrocytes. Thus, Th1-dominant inflammatory states disrupt astrocytic intercellular communication and may exacerbate MS.
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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.