ArticleJournal of neuro-oncology2008
Intracellular application of TNF-alpha impairs cell to cell communication via gap junctions in glioma cells.
Article in Journal of neuro-oncology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 27 citations in OpenAlex.
- Connexin 43: An Interface Connecting Neuroinflammation to Depression.Molecules (Basel, Switzerland) · 2023Review
- Connexins, Pannexins and Gap Junctions in Perinatal Brain Injury.Biomedicines · 2022Review
- How Cells Communicate with Each Other in the Tumor Microenvironment: Suggestions to Design Novel Therapeutic Strategies in Cancer Disease.International journal of molecular sciences · 2021Review
- Correlation of higher levels of soluble TNF-R1 with a shorter survival, independent of age, in recurrent glioblastoma.Journal of neuro-oncology · 2017Article
- Th1 cells downregulate connexin 43 gap junctions in astrocytes via microglial activation.Scientific reports · 2016Article
- Gap junction proteins and their role in spinal cord injury.Frontiers in molecular neuroscience · 2014Review
- Effect of chronic intracerebroventricluar administration of lipopolysaccharide on connexin43 protein expression in rat hippocampus.Iranian biomedical journal · 2012Article
- Dexamethasone differentially regulates functional membrane properties in glioma cell lines and primary astrocytes in vitro.Journal of neuro-oncology · 2011Article
- Neuroinflammation leads to region-dependent alterations in astrocyte gap junction communication and hemichannel activity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011Article
- Article
- Modulation of brain hemichannels and gap junction channels by pro-inflammatory agents and their possible role in neurodegeneration.Antioxidants & redox signaling · 2009Review
- Glial connexins and gap junctions in CNS inflammation and disease.Journal of neurochemistry · 2008Review
- Connexins and their channels in inflammation.Critical reviews in biochemistry and molecular biologyReview
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human gliomas are the most common class of brain neoplasm. In order to better characterize their response to inflammation, we evaluated the influence of tumor necrosis factor alpha (TNF-alpha) on the coupling behaviour and the membrane resting potential (MRP) of glioma cells (F98 glioma cell line) compared to primary astrocytes. In contrast to cultured primary astrocytes which exhibited a profound inhibition of gap junction mediated intercellular communication (GJIC), extracellular exposure of TNF-alpha to F98 glioma cells gained no effect on the functional coupling. Whereas, intracellular application of TNF-alpha into the glioma cells elicited similar effects as those found in primary astrocytes indicating a compromised accessibility of the TNF-alpha receptor in F98 cells. Western blotting, immunocytochemical staining and real time RT PCR analysis revealed a differential expression and distribution of TNF-alpha receptor 1 (TNFR1) in the glioma cells. Connexin 43 (Cx43) is the major astrocytic gap junction protein which when phosphorylated has been shown to reveal altered gating properties. Here we show that TNF-alpha increases the level of phosphorylated Cx43 in primary astrocytes but not in the F98 glioma cells. Our observations could account for the decreased regulatory effects of TNF-alpha on GJIC of F98 glioma cells.
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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.