ArticleJournal of molecular neuroscience : MN2011
Differential roles of PKA and Epac on the production of cytokines in the endotoxin-stimulated primary cultured microglia.
Article in Journal of molecular neuroscience : MN, 2011. 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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Who cites it
14 citing papers in PubMed, 23 citations in OpenAlex.
- TREM2 deficiency causes region-specific brain effects in a mouse model of cerebral amyloid angiopathy.bioRxiv : the preprint server for biology · 2026Article
- Adenylyl cyclase 2 expression and function in neurological diseases.CNS neuroscience & therapeutics · 2024Review
- Unleashing Spinal Cord Repair: The Role of cAMP-Specific PDE Inhibition in Attenuating Neuroinflammation and Boosting Regeneration after Traumatic Spinal Cord Injury.International journal of molecular sciences · 2023Review
- Inhibition of phosphodiesterase-4 in the spinal dorsal horn ameliorates neuropathic pain via cAMP-cytokine-Cx43 signaling in mice.CNS neuroscience & therapeutics · 2022Article
- βLung · 2021Article
- Epac1 deficiency inhibits basic fibroblast growth factor-mediated vascular smooth muscle cell migration.The journal of physiological sciences : JPS · 2019Article
- Protective Effect of Quercetin in LPS-Induced Murine Acute Lung Injury Mediated by cAMP-Epac Pathway.Inflammation · 2018Article
- A G protein-coupled α7 nicotinic receptor regulates signaling and TNF-α release in microglia.FEBS open bio · 2017Article
- Epac1 agonist decreased inflammatory proteins in retinal endothelial cells, and loss of Epac1 increased inflammatory proteins in the retinal vasculature of mice.Molecular vision · 2017Article
- Balancing the immune response in the brain: IL-10 and its regulation.Journal of neuroinflammation · 2016Review
- siRNA-mediated silencing of phosphodiesterase 4B expression affects the production of cytokines in endotoxin-stimulated primary cultured microglia.Experimental and therapeutic medicine · 2016Article
- Neuroprotective role of prostaglandin PGE2 EP2 receptor in hemin-mediated toxicity.Neurotoxicology · 2015Article
- EP2 receptor signaling pathways regulate classical activation of microglia.The Journal of biological chemistry · 2013Article
- Can the anti-inflammatory activities of β2-agonists be harnessed in the clinical setting?Drug design, development and therapy · 2013Review
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
To further understand the anti-inflammatory effect of adenosine cyclic 3',5'-monophosphate (cAMP), we examined the effect of protein kinase A (PKA) and cAMP-responsive guanine nucleotide exchange factor (Epac) on the transcription and production of cytokines and on the activity of mitogen-activated protein kinases (MAPK) p38 and glycogen synthase kinase-3β (GSK-3β) in endotoxin-treated rat primary cultured microglia. The PKA specific agonist N6-benzoyladenosine-3,5-cAMP (6-Bnz-cAMP) not only inhibited the transcription and production of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) but also enhanced the transcription and expression of IL-10, while the Epac selective analog 8-(4-chlorophenylthio)-2-O-methyladenosine-3,5-cAMP (8-pCPT-2'-O-Me-cAMP) merely repressed the TNF-α expression. Western blots assays indicated that 6-Bnz-cAMP significantly inhibited lipopolysaccharide-induced activation of both p38 and GSK-3β in a dose-dependent manner; in contrast, 8-pCPT-2'-O-Me-cAMP only slightly repressed GSK-3β activity at large doses. Pretreatment with H-89, a specific PKA antagonist, could completely reverse the effect of 6-Bnz-cAMP on cytokines expressions and kinases activities but had no effect on the performance of 8-pCPT-2'-O-Me-cAMP. Our findings indicate that PKA and Epac exert differential effect on the expression of inflammatory cytokines such as TNF-α, IL-1β, and IL-10, possibly owing to the different effects on the downstream effectors, MAPK p38, and GSK-3β.
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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.