ArticleNeuroscience bulletin2015
Decreased connexin 43 in astrocytes inhibits the neuroinflammatory reaction in an acute mouse model of neonatal sepsis.
Article in Neuroscience bulletin, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
12 citing papers in PubMed, 16 citations in OpenAlex.
- Review
- Article
- Astroglia in Sepsis Associated Encephalopathy.Neurochemical research · 2020Review
- The Multifaceted Role of Astrocyte Connexin 43 in Ischemic Stroke Through Forming Hemichannels and Gap Junctions.Frontiers in neurology · 2020Review
- Connexins in Astrocyte Migration.Frontiers in pharmacology · 2019Review
- A connexin43/YAP axis regulates astroglial-mesenchymal transition in hemoglobin induced astrocyte activation.Cell death and differentiation · 2018Article
- Roles of astrocytic connexin-43, hemichannels, and gap junctions in oxygen-glucose deprivation/reperfusion injury induced neuroinflammation and the possible regulatory mechanisms of salvianolic acid B and carbenoxolone.Journal of neuroinflammation · 2018Article
- Connexin 43 Controls the Astrocyte Immunoregulatory Phenotype.Brain sciences · 2018Article
- Brain Barrier Breakdown as a Cause and Consequence of Neuroinflammation in Sepsis.Molecular neurobiology · 2018Review
- The role of connexin and pannexin containing channels in the innate and acquired immune response.Biochimica et biophysica acta. Biomembranes · 2018Review
- TLR signaling adaptor protein MyD88 in primary sensory neurons contributes to persistent inflammatory and neuropathic pain and neuroinflammation.Scientific reports · 2016Article
- Neuroinflammation.Neuroscience bulletin · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neonatal sepsis is common in neonatal intensive care units, often complicated by injury to the immature brain. Previous studies have shown that the expression of the gap junction protein connexin 43 (Cx43) in the brain decreases when stimulated by neuro-inflammatory drugs such as lipopolysaccharide (LPS). Here we showed that partial deletion of Cx43 in astrocytes resulted in weakened inflammatory responses. The up-regulation of pro-inflammatory cytokines was significantly reduced in mice with partial deletion of Cx43 in astrocytes compared with wild-type littermates after systemic LPS injection. Moreover, microglial activation was inhibited in mice with partial deletion of Cx43. These results showed that Cx43 in astrocytes plays a critical role in neuro-inflammatory responses. This work provides a potential therapeutic target for inhibiting neuro-inflammatory responses in neonatal sepsis.
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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.