ArticleJournal of neuroimmunology2012
Loss of astrocyte connexins 43 and 30 does not significantly alter susceptibility or severity of acute experimental autoimmune encephalomyelitis in mice.
Article in Journal of neuroimmunology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
18 citing papers in PubMed, 30 citations in OpenAlex.
- A Brain Endothelial Cell Caveolin-1/CXCL10 Axis Promotes T Cell Transcellular Migration Across the Blood-Brain Barrier.ASN neuro · 2025Article
- Mechanistic insights into connexin-mediated neuroglia crosstalk in neurodegenerative diseases.Frontiers in cellular neuroscience · 2025Review
- Connexins Control Glial Inflammation in Various Neurological Diseases.International journal of molecular sciences · 2023Review
- Connexin 43: An Interface Connecting Neuroinflammation to Depression.Molecules (Basel, Switzerland) · 2023Review
- Targeting gliovascular connexins prevents inflammatory blood-brain barrier leakage and astrogliosis.JCI insight · 2022Article
- Oligodendroglial connexin 47 regulates neuroinflammation upon autoimmune demyelination in a novel mouse model of multiple sclerosis.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Blood-Brain Barrier: From Physiology to Disease and Back.Physiological reviews · 2019Review
- Beneficial and Detrimental Remodeling of Glial Connexin and Pannexin Functions in Rodent Models of Nervous System Diseases.Frontiers in cellular neuroscience · 2019Article
- Function of Connexins in the Interaction between Glial and Vascular Cells in the Central Nervous System and Related Neurological Diseases.Neural plasticity · 2018Review
- Connexin 30 Deficiency Attenuates Chronic but Not Acute Phases of Experimental Autoimmune Encephalomyelitis Through Induction of Neuroprotective Microglia.Frontiers in immunology · 2018Article
- Caveolin1 Is Required for Th1 Cell Infiltration, but Not Tight Junction Remodeling, at the Blood-Brain Barrier in Autoimmune Neuroinflammation.Cell reports · 2017Article
- Endothelial Wnt/β-catenin signaling reduces immune cell infiltration in multiple sclerosis.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Astrocytic Cx 43 and Cx 40 in the mouse hippocampus during and after pilocarpine-induced status epilepticus.Experimental brain research · 2015Article
- Loss of Allograft Inflammatory Factor-1 Ameliorates Experimental Autoimmune Encephalomyelitis by Limiting Encephalitogenic CD4 T-Cell Expansion.Molecular medicine (Cambridge, Mass.) · 2015Article
- Gap junctions and hemichannels composed of connexins: potential therapeutic targets for neurodegenerative diseases.Frontiers in cellular neuroscience · 2014Review
- Neurological manifestations of oculodentodigital dysplasia: a Cx43 channelopathy of the central nervous system?Frontiers in pharmacology · 2013Review
- Brain connexins in demyelinating diseases: therapeutic potential of glial targets.Brain research · 2012Review
- Connexins and their channels in inflammation.Critical reviews in biochemistry and molecular biologyReview
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
We showed previously that mice deficient in astrocyte gap junctions Cx43 and Cx30 exhibit white matter vacuolation and hypomyelination. In this study we tested the hypothesis that loss of astrocytic gap junction proteins leads to exacerbation of the primary demyelinating diseases, using experimental autoimmune encephalomyelitis (EAE) as a model system. To test for this, Cx43 floxed mice were crossed with GFAP:Cre, Cx30 null mice to generate mice lacking astrocytic expression of both Cx43 and Cx30 (dKO). EAE was induced using myelin oligodendrocyte glycoprotein (MOG(35-55)) peptide, and mice were monitored for acute expression of disease. No statistically significant difference in clinical or pathological expression of EAE was observed. Lesion load and susceptibility of different areas of the CNS to inflammation were similar in all genotypes. Moreover, no differences were noted in blood-brain barrier (BBB) permeability, tissue wet weight, axonal pathology, gliosis or demyelination during acute disease. These data show that loss of the astrocytic connexins, Cx43 and Cx30, and the white matter pathology observed in these mice does not statistically affect clinical or pathological expression of EAE and show that astrocyte gap junctions do not regulate autoimmune inflammation and associated BBB disruption in acute EAE.
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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.