ArticleJournal of neurochemistry1998
Prostaglandin E2 and 4-aminopyridine prevent the lipopolysaccharide-induced outwardly rectifying potassium current and interleukin-1beta production in cultured rat microglia.
Article in Journal of neurochemistry, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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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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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
14 citing papers in PubMed, 55 citations in OpenAlex.
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- Prostaglandins and inflammation.Arteriosclerosis, thrombosis, and vascular biology · 2011Review
- Strategies for study of neuroprotection from cold-preconditioning.Journal of visualized experiments : JoVE · 2010Article
- A role for potassium permeability in the recognition, clearance, and anti-inflammatory effects of apoptotic cells.Molecular neurobiology · 2010Article
- The prostaglandin E2 E-prostanoid 4 receptor exerts anti-inflammatory effects in brain innate immunity.Journal of immunology (Baltimore, Md. : 1950) · 2010Article
- The action of prostaglandins on ion channels.Current neuropharmacology · 2006Article
- Inhibition of microglial inflammatory responses by norepinephrine: effects on nitric oxide and interleukin-1beta production.Journal of neuroinflammation · 2004Article
- A novel mechanism of dendritic spine plasticity involving estradiol induction of prostaglandin-E2.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2002Article
- In vivo indomethacin treatment causes microglial activation in adult mice.Neurochemical research · 2000Article
- Prostaglandin E receptor subtypes in cultured rat microglia and their role in reducing lipopolysaccharide-induced interleukin-1beta production.Journal of neurochemistry · 1999Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Brain inflammation includes microglial activation and enhanced production of diffusible chemical mediators, including prostaglandin E2. Prostaglandin E2 is generally considered a proinflammatory molecule, but it also promotes neuronal survival and down-regulates some aspects of microglial activation. It remains unknown, however, if and how prostaglandin E2 prevents microglial activation. In primary culture, microglial activation is predicted by a characteristic pattern of whole-cell potassium currents and interleukin-1beta production. We investigated if prostaglandin E2 could alter these currents and, if so, whether these currents are necessary for microglial activation. Microglia were isolated from mixed cell cultures prepared from neonatal rat brains and exposed to 0-10 microM prostaglandin E2 and lipopolysaccharide for 24 h. Currents were elicited by using standard patch-clamp technique, and interleukin-1beta production was measured by ELISA. Peak outward current densities in microglia treated with lipopolysaccharide plus prostaglandin E2 (10 nM) were reduced significantly from those of cells treated with lipopolysaccharide alone. Prostaglandin E2 and 4-aminopyridine (a blocker of outward potassium currents) also significantly reduced interleukin-1beta production. Thus, although prostaglandin E2 is classified generally as a proinflammatory chemical, it has complex roles in brain inflammation that include preventing microglial activation, perhaps by reducing the outward potassium current.
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